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Relevant bibliographies by topics / C3-convertase of alternative complement pathway

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Academic literature on the topic 'C3-convertase of alternative complement pathway'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "C3-convertase of alternative complement pathway"

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Hourcade, Dennis E., Lynne M. Mitchell, and M. Edward Medof. "Decay acceleration of the complement alternative pathway C3 convertase." Immunopharmacology 42, no. 1-3 (1999): 167–73. http://dx.doi.org/10.1016/s0162-3109(99)00005-3.

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Roumenina, Lubka T., Mathieu Jablonski, Christophe Hue, et al. "Hyperfunctional C3 convertase leads to complement deposition on endothelial cells and contributes to atypical hemolytic uremic syndrome." Blood 114, no. 13 (2009): 2837–45. http://dx.doi.org/10.1182/blood-2009-01-197640.

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Abstract Complement is a major innate immune defense against pathogens, tightly regulated to prevent host tissue damage. Atypical hemolytic uremic syndrome (aHUS) is characterized by endothelial damage leading to renal failure and is highly associated with abnormal alternative pathway regulation. We characterized the functional consequences of 2 aHUS-associated mutations (D254G and K325N) in factor B, a key participant in the alternative C3 convertase. Mutant proteins formed high-affinity C3-binding site, leading to a hyperfunctional C3 convertase, resistant to decay by factor H. This led to e

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Mullick, Jayati, John Bernet, Yogesh Panse, Sharanabasava Hallihosur, Akhilesh K. Singh, and Arvind Sahu. "Identification of Complement Regulatory Domains in Vaccinia Virus Complement Control Protein." Journal of Virology 79, no. 19 (2005): 12382–93. http://dx.doi.org/10.1128/jvi.79.19.12382-12393.2005.

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ABSTRACT Vaccinia virus encodes a homolog of the human complement regulators named vaccinia virus complement control protein (VCP). It is composed of four contiguous complement control protein (CCP) domains. Previously, VCP has been shown to bind to C3b and C4b and to inactivate the classical and alternative pathway C3 convertases by accelerating the decay of the classical pathway C3 convertase and (to a limited extent) the alternative pathway C3 convertase, as well as by supporting the factor I-mediated inactivation of C3b and C4b (the subunits of C3 convertases). In this study, we have mappe

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Schwendinger, M. G., M. Spruth, J. Schoch, M. P. Dierich, and W. M. Prodinger. "A novel mechanism of alternative pathway complement activation accounts for the deposition of C3 fragments on CR2-expressing homologous cells." Journal of Immunology 158, no. 11 (1997): 5455–63. http://dx.doi.org/10.4049/jimmunol.158.11.5455.

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Abstract Complement receptor type 2 (CD21, CR2), the receptor for the C3 fragment C3dg, activates complement via the alternative pathway and also serves as a preferential acceptor site for C3 fragments. The molecular basis for this phenomenon, which has recently been demonstrated for B lymphocytes in vivo, is currently not understood. Here we present a model for this CR2-dependent complement activation. The inactive C3 (iC3), which forms spontaneously in serum in low amounts by reaction of native C3 with H2O, binds noncovalently to the N-terminal part of CR2. Subsequent association of properdi

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Chauvet, Sophie, Romain Berthaud, Magali Devriese, et al. "Anti-Factor B Antibodies and Acute Postinfectious GN in Children." Journal of the American Society of Nephrology 31, no. 4 (2020): 829–40. http://dx.doi.org/10.1681/asn.2019080851.

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BackgroundThe pathophysiology of the leading cause of pediatric acute nephritis, acute postinfectious GN, including mechanisms of the pathognomonic transient complement activation, remains uncertain. It shares clinicopathologic features with C3 glomerulopathy, a complement-mediated glomerulopathy that, unlike acute postinfectious GN, has a poor prognosis.MethodsThis retrospective study investigated mechanisms of complement activation in 34 children with acute postinfectious GN and low C3 level at onset. We screened a panel of anticomplement protein autoantibodies, carried out related functiona

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Weiler, J. M., R. E. Edens, and G. J. Gleich. "Eosinophil granule cationic proteins regulate complement. I. Activity on the alternative pathway." Journal of Immunology 149, no. 2 (1992): 643–48. http://dx.doi.org/10.4049/jimmunol.149.2.643.

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Abstract Eosinophil granules contain several cationic proteins that mediate tissue damage in allergic disease. The present study examined the capacity and mechanisms by which these cationic proteins regulate activity of the alternative pathway of C. Eosinophil peroxidase and eosinophil cationic protein inhibited formation of cell-bound alternative pathway C3 convertase, causing 50% inhibition of lysis at about 0.19 and 0.75 microgram/10(7) cellular intermediates, respectively. Major basic protein inhibited alternative pathway C3 activity by only 19% at 1.5 micrograms/10(7) cellular intermediat

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Irmscher, Sarah, Nadia Döring, Luke D. Halder, et al. "Kallikrein Cleaves C3 and Activates Complement." Journal of Innate Immunity 10, no. 2 (2017): 94–105. http://dx.doi.org/10.1159/000484257.

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The human plasma contact system is an immune surveillance system activated by the negatively charged surfaces of bacteria and fungi and includes the kallikrein-kinin, the coagulation, and the fibrinolytic systems. Previous work shows that the contact system also activates complement, and that plasma enzymes like kallikrein, plasmin, thrombin, and FXII are involved in the activation process. Here, we show for the first time that kallikrein cleaves the central complement component C3 directly to yield active components C3b and C3a. The cleavage site within C3 is identical to that recognized by t

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Pangburn, M. K., and H. J. Müller-Eberhard. "The C3 convertase of the alternative pathway of human complement. Enzymic properties of the bimolecular proteinase." Biochemical Journal 235, no. 3 (1986): 723–30. http://dx.doi.org/10.1042/bj2350723.

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The association of Factor B with C3b (the major fragment of complement component C3) in the presence of Mg2+ results in the formation of a bimolecular zymogen, C3b,B, which is activated by the serine proteinase Factor D, generating the C3 convertase, C3b,Bb (EC 3.4.21.47). Cleavage of native C3 by the C3 convertase was monitored by recording the increase in fluorescence associated with C3b formation in the presence of the fluorescent probe 8-anilinonaphthalene-1-sulphonate. Measurements of initial rates of C3b formation at various C3 concentrations were analysed in accordance with the Michaeli

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Sahu, Arvind, Stuart N. Isaacs, Athena M. Soulika, and John D. Lambris. "Interaction of Vaccinia Virus Complement Control Protein with Human Complement Proteins: Factor I-Mediated Degradation of C3b to iC3b1 Inactivates the Alternative Complement Pathway." Journal of Immunology 160, no. 11 (1998): 5596–604. http://dx.doi.org/10.4049/jimmunol.160.11.5596.

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Abstract Vaccinia virus complement control protein (VCP) is a virulence determinant of vaccinia virus that helps protect the virus from the complement attack of the host. To characterize the interaction of VCP with C3 and C4 and understand the mechanism by which VCP inactivates complement, we have expressed VCP in a yeast expression system and compared the biologic activity of the purified protein to that of human factor H and complement receptor 1 (CR1). Recombinant VCP bound to C3 and the proteolytically cleaved form of C3 (C3b), but not to the 135,300-m.w. fragment of C3 generated using ela

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Jiang, Haixiang, Eric Wagner, Huamei Zhang, and Michael M. Frank. "Complement 1 Inhibitor Is a Regulator of the Alternative Complement Pathway." Journal of Experimental Medicine 194, no. 11 (2001): 1609–16. http://dx.doi.org/10.1084/jem.194.11.1609.

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We studied complement 1 inhibitor (C1-INH) as an inhibitor of the alternative complement pathway. C1-INH prevented lysis, induced by the alternative complement pathway, of paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes in human serum. It inhibited the binding of both factors B and C3 to PNH and rabbit erythrocytes and blocked the ability of factor B to restore alternative-pathway function in factor B–depleted serum. C1-INH did not bind to factors B or D but did bind to immobilized C3b and cobra venom factor (CVF), a C3b analogue. C1-INH prevented factor B from binding to CVF-coated bea

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Dissertations / Theses on the topic "C3-convertase of alternative complement pathway"

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Marinozzi, Maria Chiara. "Characterization of the complement hereditary and acquired abnormalities in atypical Hemolytic Uremic Syndrome and C3 Glomerulopathy." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB037/document.

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Harris, Claire Louise. "Analysis of covalent binding reactions between human complement component C3 and other proteins of the alternative pathway." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309802.

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DI, FEDE MARTINA. "Dissecting the role of Neisseria Heparin Binding Antigen cleavage during adaptation of Neisseria meningitidis to mucosal surface." Doctoral thesis, Università di Siena, 2017. http://hdl.handle.net/11365/1009815.

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Neisserial Heparin Binding Antigen (NHBA) is a surface-exposed lipoprotein specific for Neisseria and is one of the three main protein antigens of the Bexsero vaccine. Meningococcal and human proteases, including lactoferrin and kallikrein, cleave NHBA protein upstream or downstream a conserved Arg-rich motif, respectively. The cleavage results in the release of the C-terminal portion of the protein. C-terminal fragment originating from the processing of meningococcal proteases, referred as C2 fragment, exerts a toxic effect on endothelial cells altering their permeability. In this work, we re

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Praz, Françoise. "Effets de l'activation du systeme du complement sur differentes populations lymphocytaires." Paris 6, 1987. http://www.theses.fr/1987PA066589.

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Garnier, Gérard. "Le facteur B du complément humain : bases structurales et biosynthétiques de sa microhétérogénéité, mises en évidence par les techniques électrophorétiques." Rouen, 1988. http://www.theses.fr/1988ROUES026.

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Iferroudjene, Djedjiga. "Complément et réponse immune : effet comitogénique du composant C3 et du facteur H sur les lymphocytes T." Rouen, 1988. http://www.theses.fr/1988ROUES011.

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Books on the topic "C3-convertase of alternative complement pathway"

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Medjeral-Thomas, Nicholas, Anna Richards, and Matthew C. Pickering. Molecular basis of complement-mediated renal disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0333.

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Abnormal regulation of complement is intimately associated with C3 glomerulopathy and atypical haemolytic uraemic syndrome. Atypical haemolytic uraemic syndrome is characterized by renal thrombotic microangiopathy due to an inability to regulate complement activation along the renal endothelium. The development of thrombosis is critically dependent on the ability to activate C5. Eculizumab, a monoclonal anti-C5 antibody, is an effective therapy for this condition. C3 glomerulopathy refers to glomerular lesions characterized by accumulation of C3 in the absence of immunoglobulin. The prototypic

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Book chapters on the topic "C3-convertase of alternative complement pathway"

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Michels, Marloes A. H. M., Nicole C. A. J. van de Kar, Elena B. Volokhina, and Bert(L) P. W. J. van den Heuvel. "Functional Hemolytic Test for Complement Alternative Pathway Convertase Activity." In The Complement System. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1016-9_8.

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Densen, P., C. McRill, and S. C. Ross. "The contribution of the alternative and classical complement pathways to gonococcal killing and C3 fixation." In Gonococci and Meningococci. Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1383-7_108.

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Turner-Stokes, Tabitha, and Mark A. Little. "Membranoproliferative glomerulonephritis." In Oxford Textbook of Medicine, edited by John D. Firth. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0487.

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The key histological features of membranoproliferative glomerulonephritis (MPGN) are mesangial hypercellularity, endocapillary proliferation, and capillary wall remodelling. There are two main types: (1) immune complex-mediated disease—caused by chronic infection causing persistent antigenaemia (notably hepatitis C), autoimmune disease, or monoclonal immunoglobulin production by plasma cell dyscrasia, and a few ‘idiopathic’ cases; and (2) complement-mediated disease—caused by dysregulation of the alternative pathway of complement, including by C3 nephritic factor (C3Nef), an autoantibody that stabilizes the alternative pathway C3 convertase. Clinical presentation is varied, including nephrotic syndrome, episodic visible haematuria, hypertension/rapidly progressive glomerulonephritis, asymptomatic nonvisible haematuria, and chronic kidney disease. Treatment depends on the underlying disease. All patients should receive appropriate conservative measures (blood pressure control, angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker). Underlying infection or monoclonal gammopathy should be treated, when possible, in those with immune complex-mediated MPGN. Eculizumab may have a role in treatment of some patients with complement-mediated MPGN. Steroids and cyclophosphamide or mycophenolate mofetil are used in patients with severe idiopathic MPGN.

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Vuković Brinar, Ivana, and Matija Matošević. "Complement-Mediated Kidney Disease." In Novel Topics in the Diagnosis, Treatment, and Follow-Up of Nephritis, Nephrotic Syndrome, and Nephrosis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108555.

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From very discovery of the complement cascade, it had an intriguing role in pathophysiology of kidney disease. The hallmark of complement cascade involvement in kidney diseases comprises of immune-complexes deposits in the glomeruli, acting as activation for the classical pathway. However, additional mechanisms of complement activation, namely alternative and lectin pathways are extremely important and prominent in complement-mediated kidney disease. Disease prototype of activation of complement is an atypical hemolytic uremic syndrome with solid activation of complement and C3 glomerulopathy is a hallmark of fluid phase activation of alternative complement pathway. Further research has shown that alternative pathway also plays a role in pathogenesis and progression of other kidney diseases including anti-neutrophil cytoplasmic antibody-associated vasculitis and immune complex-mediated glomerulonephritis as well as IgA nephropathy. A better understanding of complement system’s role in kidney disease has also brought forth novel therapeutic approaches in form of complement cascade inhibitors, revolutionizing the treatment of patients that were faced with unfavorable outcomes. Through this chapter, we bring to you an overview of most prevalent complement-mediated kidney diseases with emphasis on the role of complement in their pathogenesis and the potential for treatment targeting the complement cascade.

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Kerr, Michael A. "Factor B and the Alternative Pathway C3/C5 Convertase." In Handbook of Proteolytic Enzymes. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-382219-2.00635-9.

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Conference papers on the topic "C3-convertase of alternative complement pathway"

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Devine, D. V., and W. F. Rosse. "PLATELET FACTOR H REGULATES THE ACTIVITY OF THE ALTERNATIVE PATHWAY OF COMPLEMENT ON THE SURFACE OF NORMAL AND PAROXYSMAL NOCTURNAL HEMOGLOBINURIA PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643979.

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Paroxysmal nocturnal hemoglobinuria (PNH)-is frequently complicated by thrombosis. It has been suggested that the abnormal interactions of PNH platelets with complement contribute to thrombosis. Using purified complement proteins, we have previously demonstrated that the platelets from some patients with PNH do not demonstrate elevated activity of C3bBb, the alternative pathway C3 amplification enzyme complex, even though they lack the C3bBb regulatory protein, decay accelerating factor (DAF). As measured by fluorescence flow cytometry, washed platelets from both normal donors and PNH patients

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Naji, Foziyeh Esmaiel, Mohammed Ehlayel, Nader Al-Dewik, and Ahmed Malki. "Clinical Utility and Cost Effectiveness of Complement 3 and Complement 4 in different Clinical Subspecialties in Hamad Medical Corporation." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0161.

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Background: Complement system is one of ancient innate immune systems in our body fighting against pathogens and foreign bodies. Either one of its three pathways, classical, alternative or lectin activates it. Because of its role and importance in combating against different pathological conditions, it works through defined proteins including regulators and inhibitors. However, over or under stimulation of complement system can lead to various diseases. A number of analytical assays are used to measure complement proteins and its activation states considering complement 3 (C3), complement 4 (C

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