Academic literature on the topic 'Annexin A5'
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Journal articles on the topic "Annexin A5"
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Brachvogel, Bent, Jörg Dikschas, Helga Moch, Heike Welzel, Klaus von der Mark, Clementine Hofmann, and Ernst Pöschl. "Annexin A5 Is Not Essential for Skeletal Development." Molecular and Cellular Biology 23, no. 8 (April 15, 2003): 2907–13. http://dx.doi.org/10.1128/mcb.23.8.2907-2913.2003.
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ABSTRACT Annexins are highly conserved proteins that are characterized by their ability to interact with phospholipids in a calcium-dependent manner. Although diverse functions have been ascribed to annexins based on in vitro analyses, their in vivo functions still remain unclear. The intensively studied annexin A5 has been identified by its effects on blood coagulation, and subsequently, its function as a calcium-specific ion channel was described. In vitro experiments and expression studies suggested a potential role of annexin A5 during calcification processes in vivo, especially in endochondral ossification. To gain insights into the relevance of annexin A5 in this process, we generated an annexin A5-deficient mouse mutant. Mice lacking annexin A5 are viable, are fertile, and reveal no significant alterations in the biochemical parameters characteristic for metabolic or functional defects. Neither the development of skeletal elements nor the in vitro calcification properties of isolated chondrocytes is significantly impaired by the absence of annexin A5. Therefore, annexin A5 is dispensable for the formation and maintenance of skeletal elements in the mouse and may possibly be pointing to a compensatory effect of other members from the annexin family due to their high functional and structural similarity.
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BROOKS, Nicole D., Jean E. GRUNDY, Nadine LAVIGNE, Mélanie C. DERRY, Christina M. RESTALL, ROGER C. MacKENZIE, David M. WAISMAN, and Edward L. G. PRYZDIAL. "Ca2+-dependent and phospholipid-independent binding of annexin 2 and annexin 5." Biochemical Journal 367, no. 3 (November 1, 2002): 895–900. http://dx.doi.org/10.1042/bj20020997.
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Annexins are a family of homologous proteins that associate with anionic phospholipid (aPL) in the presence of Ca2+. Evidence that the function of one annexin type may be regulated by another was recently reported in studies investigating cytomegalovirus—aPL interactions, where the fusogenic function of annexin 2 (A2) was attenuated by annexin 5 (A5). This observation suggested that A2 may bind directly to A5. In the present study, we demonstrated this interaction. The A2—A5 complex was first detected utilizing (covalently linked) fluorescein-labelled A5 (F-A5) as a reporter group. The interaction required concentrations of Ca2+ in the millimolar range, had an apparent dissociation constant [Kd(app)] of 1nM at 2mM Ca2+ and was independent of aPL. A2 bound comparably with F-A5 pre-equilibrated with an amount of aPL that could bind just the F-A5 or to an excess amount of aPL providing sufficient binding sites for all of F-A5 and A2. A2—A5 complex formation was corroborated in an experiment, where [125I]A2 associated in a Ca2+-dependent manner with A5 coated on to polystyrene. Surface plasmon resonance was used as a third independent method to demonstrate the binding of A2 and A5 and, furthermore, supported the conclusion that the monomeric and tetrameric forms of A2 bind equivalently to A5. Together these results demonstrate an A2—A5 interaction and provide an explanation as to how A5 inhibits the previously reported A2-dependent enhancement of virus—aPL fusion.
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Bećarević, Mirjana, Svetlana Ignjatović, and Nada Majkić-Singh. "Apoptosis, Annexin A5 and Anti-Annexin A5 Antibodies in The Antiphospholipid Syndrome." Journal of Medical Biochemistry 32, no. 2 (April 1, 2013): 89–95. http://dx.doi.org/10.2478/jomb-2013-0014.
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Summary It has been proposed that apoptosis is one of the mechanisms involved in the generation of antiphospholipid antibodies. The presence of antiphospholipid antibodies is the main laboratory criterion for a definite diagnosis of the antiphospholipid syndrome. Annexinopathies are disorders characterized by deregulation of annexins expression levels and function. Annexin A5 has been used as an agent for molecular imaging techniques (visualization of phosphatidylserineexpressing apoptotic cells) in vitro and in vivo in animal models and in patients (injection of human recombinant anxA5 into the patient‘s circulation). Although the determination of titers of anti-annexin A5 antibodies is not mandatory for the diagnosis of the antiphospholipid syndrome, it was reported that patients with primary antiphospholipid syndrome with a history of recurrent abortions had elevated titers of antiannexin A5 antibodies, while the presence of thromboses was not associated with elevated levels of these antibodies
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Hu, Guochang. "Recombinant Human Annexin A5." Critical Care Medicine 42, no. 1 (January 2014): 219–20. http://dx.doi.org/10.1097/01.ccm.0000435680.21801.0f.
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Derry, Mélanie C., Michael R. Sutherland, Christina M. Restall, David M. Waisman, and Edward L. G. Pryzdial. "Annexin 2-mediated enhancement of cytomegalovirus infection opposes inhibition by annexin 1 or annexin 5." Journal of General Virology 88, no. 1 (January 1, 2007): 19–27. http://dx.doi.org/10.1099/vir.0.82294-0.
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Biochemical studies have suggested that annexin 2 (A2) may participate in cytomegalovirus (CMV) infection. In the current work, effects of A2 monomer (p36) and heterotetramer (A2t; p362p112) were investigated. Demonstrating a role for endogenous A2, the four stages of infection that were followed were each inhibited by anti-p36 or anti-p11 at 37 °C. Immuno-inhibition was attenuated when the virus and cells were pre-incubated at 4 °C to coordinate virus entry initiated afterwards at 37 °C, reconciling controversy in the literature. As an explanation, CMV-induced phosphorylation of p36 was prevented by the 4 °C treatment. Supporting these immuno-inhibition data, purified A2t or p11 increased CMV infectious-progeny generation and CMV gene expression. A specific role for A2t was indicated by purified p36 having no effect. Unlike other steps, primary plaque formation was not enhanced by purified A2t or p11, possibly because of undetectable phosphorylation. As annexins 1 (A1) and 5 (A5) interact with A2, their effect on CMV was also tested. Both purified proteins inhibited CMV infection. In each experiment, the concentration of A1 required for half-maximal inhibition was five- to 10-fold lower than that of A5. Addition of A2 opposed A1- or A5-mediated inhibition of CMV, as did certain A2-specific antibodies that had no effect in the absence of added A1 or A5. Transfection of the p36-deficient cell line HepG2 increased CMV infection and was required for inhibition by the other annexins. These data suggest that CMV exploits A2t at physiological temperature to oppose the protection of cells conferred by A1 or A5.
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Monastyrskaya, Katia, Fabian Tschumi, Eduard B. Babiychuk, Deborah Stroka, and Annette Draeger. "Annexins sense changes in intracellular pH during hypoxia." Biochemical Journal 409, no. 1 (December 11, 2007): 65–75. http://dx.doi.org/10.1042/bj20071116.
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The pHi (intracellular pH) is an important physiological parameter which is altered during hypoxia and ischaemia, pathological conditions accompanied by a dramatic decrease in pHi. Sensors of pHi include ion transport systems which control intracellular Ca2+ gradients and link changes in pHi to functions as diverse as proliferation and apoptosis. The annexins are a protein family characterized by Ca2+-dependent interactions with cellular membranes. Additionally, in vitro evidence points to the existence of pH-dependent, Ca2+-independent membrane association of several annexins. We show that hypoxia promotes the interaction of the recombinant annexin A2–S100A10 (p11) and annexin A6 with the plasma membrane. We have investigated in vivo the influence of the pHi on the membrane association of human annexins A1, A2, A4, A5 and A6 tagged with fluorescent proteins, and characterized this interaction for endogenous annexins present in smooth muscle and HEK (human embryonic kidney)-293 cells biochemically and by immunofluorescence microscopy. Our results show that annexin A6 and the heterotetramer A2–S100A10 (but not annexins A1, A4 and A5) interact independently of Ca2+ with the plasma membrane at pH 6.2 and 6.6. The dimerization of annexin A2 within the annexin A2–S100A10 complex is essential for the pH-dependent membrane interaction at this pH range. The pH-induced membrane binding of annexins A6 and A2–S100A10 might have consequences for their functions as membrane organizers and channel modulators.
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Bahmani, Peyman, Eyk Schellenberger, Jan Klohs, Jens Steinbrink, Ryan Cordell, Marietta Zille, Jochen Müller, et al. "Visualization of Cell Death in MICE with Focal Cerebral Ischemia using Fluorescent Annexin A5, Propidium Iodide, and Tunel Staining." Journal of Cerebral Blood Flow & Metabolism 31, no. 5 (January 19, 2011): 1311–20. http://dx.doi.org/10.1038/jcbfm.2010.233.
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To monitor stroke-induced brain damage and assess neuroprotective therapies, specific imaging of cell death after cerebral ischemia in a noninvasive manner is highly desirable. Annexin A5 has been suggested as a marker for imaging cell death under various disease conditions including stroke. In this study, C57BL6/N mice received middle cerebral artery occlusion (MCAO) and were injected intravenously with either active or inactive Cy5.5-annexin A5 48 hours after reperfusion. Some mice also received propidium iodide (PI), a cell integrity marker. Only in mice receiving active Cy5.5-annexin A5 were fluorescence intensities significantly higher over the hemisphere ipsilateral to MCAO than on the contralateral side. This was detected noninvasively and ex vivo 4 and 8 hours after injection. The majority of cells positive for fluorescent annexin A5 were also positive for PI and fragmented DNA as detected by terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling (TUNEL) staining. This study demonstrates the high specificity of annexin A5 for visualization of cell death in a mouse model of stroke. To our knowledge, this is the first study to compare the distribution of injected active and inactive annexin A5, PI, and TUNEL staining. It provides important information on the experimental and potential clinical applications of annexin A5-based imaging agents in stroke.
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Hiddink, Larissa, Marieke C. H. de Visser, and Waander L. van Heerde. "Polymorphisms in the Annexin A5 gene influence circulating Annexin A5 levels in healthy controls." Thrombosis Research 129, no. 6 (June 2012): 815–17. http://dx.doi.org/10.1016/j.thromres.2012.03.022.
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Baleva, Marta, Maria Hristova, and Krasimir Nikolov. "Diagnostic significance of anti-annexin-A5 antibody determination." Open Medicine 5, no. 1 (February 1, 2010): 6–11. http://dx.doi.org/10.2478/s11536-009-0132-4.
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AbstractAnti-annexin A5 antibodies are directed against annexin A5 — a phospholipid-binding protein that belongs to the ubiquitous annexin family. These antibodies were first discovered in 1994 by Matsuda et al. in women with recurrent fetal loss or preeclampsia and in patients with systemic lupus erythematosus and positive lupus anticoagulant and/or anticardiolipin antibodies. Since then anti-annexin A5 antibodies have been the focus of research. In addition to their well known prothrombotic and procoagulant activities the authors discuss the involvement of these antibodies in the pathogenesis of antiphospholipid syndrome, recurrent pregnancy loss, systemic lupus erythematosus and other immune and non-immune disorders. Controversial reports are presented and a possible interpretation of the results is given. The authors suggest the significance of anti-annexin A5 antibodies as an additional diagnostic marker and discuss the necessity of more extensive research on their clinical significance.
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Monceau, Virginie, Yulia Belikova, Gueorgui Kratassiouk, Estelle Robidel, Françoise Russo-Marie, and Daniele Charlemagne. "Myocyte apoptosis during acute myocardial infarction in rats is related to early sarcolemmal translocation of annexin A5 in border zone." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 2 (August 2006): H965—H971. http://dx.doi.org/10.1152/ajpheart.01053.2005.
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Annexin A5 is a Ca2+-dependent phospholipid binding protein well known for its high phosphatidylserine affinity. In vitro, translocation to sarcolemma and externalization of endogenous annexin A5 in the cardiomyocyte has recently been demonstrated to exert a proapoptotic effect. To determine whether these in vitro findings occurred in vivo, we performed myocardial infarction (MI) and studied the time course of apoptosis and annexin A5 localization (0.5 to 8 h) in the border zone around the infarcted area. This zone that was defined as Evans blue unstained and triphenyltetrazolium chloride (TTC) stained, represented 42.3 ± 5.5% of the area at risk and showed apoptotic characteristics (significant increases in caspase 3 activity 2.3-fold at 0.5 h; P < 0.05), transferase-mediated dUTP nick-end labeling-positive cardiomyocytes (15.8 ± 0.8% at 8 h), and DNA ladder. When compared with sham-operated rats, we found that in this area, annexin A5 was translocated to the sarcolemma as early as 0.5 h after MI and that translocation increased with time. Moreover, the amount of annexin A5 was unchanged in the border zone and decreased in the infarcted area after 1 h (77.1 ± 4.8%; P < 0.01 vs. perfused area), suggesting a release in the latter but not in the former. In conclusion, we demonstrated that annexin A5 translocation is an early and rapid event of the whole border zone, likely due to Ca2+ increase. Part of this translocation occurred in areas where apoptosis was later detected and suggests that in vivo as in vitro annexin A5 might be involved in the regulation of early apoptotic events during cardiac pathological situations.
Dissertations / Theses on the topic "Annexin A5"
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Ghislat, Cherfaoui Ghita. "Regulation of Lysosomal Degradation by CA2+And CA2+-Binding Proteins." Doctoral thesis, Universitat Politècnica de València, 2013. http://hdl.handle.net/10251/29690.
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La macroautofagia y la endocitosis son dos procesos catabólicos
conservados evolutivamente en los que, mediante un tráfico vesicular, se
degrada el material secuestrado, cuyo origen es intra- y extracelular,
respectivamente. Ambos procesos comienzan de manera diferente:
mediante la formación de un nuevo orgánulo, el autofagosoma, que
secuestra material citoplásmico (macroautofagia), o mediante la
internalización de material extracelular y de algunos componentes de la
membrana plasmática a través de vesículas endocíticas (endocitosis). Sin
embargo, los dos terminan en el mismo compartimiento: el lisosoma.
En un análisis proteómico de membranas lisosomales, purificadas a
partir de fibroblastos de ratón, identificamos tres proteínas, que se unen a
fosfolípidos de una manera dependiente de calcio, y cuyos niveles en la
membrana lisosomal aumentaban en ausencia de aminoácidos, una
condición que activa la macroautofagia. Basándonos en esos resultados
iniciales, y teniendo en cuenta que el calcio es un segundo mensajero muy
importante, decidimos: en primer lugar, abordar el papel del calcio en la
activación de la autofagia producida por el ayuno de aminoácidos, y, en
segundo lugar, investigar el papel de esas tres proteínas en el mecanismo
autofágico.
Como resultado de estos estudios, describimos en primer lugar una
nueva vía de señalización dependiente de calcio que activa la formación de
autofagosomas por los aminoácidos. Concretamente, hemos encontrado
que el ayuno de aminoácidos esenciales produce un aumento en el calcio
citosólico, procedente tanto del medio extracelular como de almacenes
intracelulares. Como consecuencia de esto, la calmodulina quinasa quinasa-
ß activa a AMPK y a mTORC1. En la última etapa de esta vía, ULK1, una
quinasa responsable de la iniciación de la autofagia, se activa para
contribuir a la formación de los autofagosomas.
Las tres proteínas identificadas en el estudio proteómico y cuyos
niveles en las membranas lisosomales aumentan en ausencia de aminoácidos son la anexina A1, la anexina A5 y la copina 1. Empleando
métodos bioquímicos y de inmunofluorescencia observamos que el ayuno
de aminoácidos causa la translocación de la anexina A5 desde el complejo
de Golgi hasta las membranas lisosomales, donde también se acumulan la
anexina A1 y la copina 1. Asimismo, demostramos por sobre-expresión y
silenciamiento de esas tres proteínas, que las tres inducen la fusión de
autofagosomas con lisosomas y que la copina 1, y en menor medida la
anexina A1, aumentan el efecto individual de la anexina A5. Finalmente, la
anexina A5 inhibe la endocitosis mientras que copina 1 la induce.
En resumen, nuestros resultados ponen de manifiesto que la
activación de la formación de autofagosomas por el ayuno de aminoácidos
es debida, al menos en parte, a una vía de señalización dependiente de
Ca2+
y que esta condición también conlleva la aceleración de la maduración
de los autofagosomas a autolisosomas a través de proteínas que unen el
Ca2+ como las anexinas A1 y A5 y la copina 1.Ghislat Cherfaoui, G. (2013). Regulation of Lysosomal Degradation by CA2+And CA2+-Binding Proteins [Tesis doctoral no publicada]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/29690
TESIS
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Carmeille, Romain. "Rôle de l'Annexine-A5 dans la réparation membranaire du muscle strié squelettique et du placenta humains." Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0354/document.
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La membrane plasmique est un assemblage supramoléculaire qui délimite la cellule. C’est une structure fine, complexe et dynamique assurant des fonctions multiples et vitales pour la cellule. Sa rupture est un évènement physiologique pour les cellules soumises à des stress mécaniques fréquents et/ou importants, comme les cellules épithéliales, les cellules endothéliales ou les cellules musculaires. Dans des conditions physiopathologiques, la membrane plasmique peut également être endommagée par l’insertion de toxines bactériennes formant des pores (PFTs, pour « pore forming toxins »). Le processus de réparation membranaire et la machinerie protéique associée sont encore mal connus. Connaître les partenaires protéiques et comprendre les mécanismes mis en jeu durant le processus de réparation de la membrane plasmique sont deux enjeux fondamentaux majeurs. En effet, il a été établi qu’une défaillance du processus de réparation membranaire pour les fibres musculaires est la cause principale de certaines dystrophies musculaires. La machinerie protéique de réparation comprend des protéines comme la dysferline, la cavéoline-3 et certaines Annexines (Anx). Les Anx appartiennent à une superfamille de protéines répandue chez la plupart des eucaryotes, qui ont la propriété commune de se lier aux membranes biologiques en présence de calcium (Ca2+). Certaines Anx, comme l’AnxA5, une fois liées aux membranes biologiques s’auto-assemblent spontanément en réseau-2D. Lors de ce travail de thèse, nous avons étudié le rôle de l’AnxA5 dans la réparation membranaire des trophoblastes placentaires et des cellules du muscle squelettique humain. Pour les deux types cellulaires, nous avons montré que l’AnxA5 est un acteur indispensable du processus de réparation membranaire dans le cas de ruptures mécaniques. En associant des approches de microscopie de fluorescence et de microscopie électronique à transmission (MET), nous avons mis en évidence que dans ces cellules, le mécanisme de réparation est principalement basé sur la formation d’un « patch » lipidique. Dans les cellules musculaires, les expériences de MET ont mis en évidence qu’un pool d’AnxA5 endogène se lie aux bords du site de rupture quelques secondes après la lésion du sarcolemme. Ceci suggère qu’après rupture de la membrane plasmique, l’augmentation locale de la concentration calcique intracellulaire provoque la liaison de l’AnxA5 spécifiquement aux bords de la région membranaire lésée où elle forme un réseau-2D. Le réseau-2D stabiliserait localement la membrane et préviendrait sa déchirure, induite par les forces de tensions exercées par le cytosquelette cortical. Nous avons également montré que l’AnxA5 ne semble pas impliquée dans la réparation de la membrane plasmique après insertion de PFTs. Ceci suggère que différents mécanismes de réparation existent et que leur mise en place dépend probablement du type ou de l’importance des dommages. Finalement nous avons étendu notre étude à des lignées cellulaires établies à partir de patients diagnostiqués comme souffrant de dystrophies des ceintures de type 2B (déficience en dysferline) et 1C (déficience en cavéoline-3), respectivement. Nous avons montré, pour ces lignées, que la déficience en dysferline ou cavéoline-3 provoque un défaut de réparation dans le cas des ruptures mécaniques de la membrane plasmique. Dans ces cellules musculaires pathologiques intactes ou endommagées, l’AnxA5 a le même comportement, ce qui suggère que l’action de l’AnxA5 est indépendante de ces protéines. A la différence des cellules déficientes en dysferline, nous avons observé que les cellules déficientes en cavéoline-3 sont capables de réparer efficacement des lésions créées par l’insertion de PFTs dans le sarcolemme. Ce résultat supporte l’hypothèse de l’existence de plusieurs mécanismes de réparation. En conclusion, ce travail montre que l’AnxA5 est un composant clé de la machinerie de réparation dans le cas des ruptures mécaniquesPlasma membrane is the supramolecular assembly that delimits the cell. It is a thin, dynamic and complex structure, ensuring multiple and vital cell functions. Its disruption is a physiological event occurring in cells submitted to frequent mechanical stresses, such as endothelial cells, epithelial cells and muscle cells. It is also a physiological event for cells exposed to pore forming bacterial toxins (PFTs). Membrane repair mechanisms and associated protein machinery are still poorly understood. This knowledge is, however, essential for obvious physiopathological issues. Indeed, a defect of membrane repair in muscle cells leads to some muscular dystrophies. Membrane repair machinery includes proteins such as dysferlin, MG-53, caveolin-3 and some Annexins (Anx). Anx belong to a superfamily of proteins widely spread in most of eukaryotes, which share the property of binding to biological membranes in the presence of calcium (Ca2+). Here, we investigated the role of AnxA5 in cell membrane repair of human trophoblastic and skeletal muscle cells. We showed that AnxA5 is required for membrane repair of mechanical damages in the two cell types. By combining fluorescence and transmission electron microscopy approaches, we evidenced that membrane repair mechanism in these cells is based on the formation of a lipid “patch”. In human muscle cells, TEM experiments revealed that a pool of endogenous AnxA5 binds to the edges of the torn sarcolemma as soon as a few seconds after membrane disruption. Our results suggest the following mechanism: triggered by the local increase in Ca2+ concentration, AnxA5 molecules bind to PS exposed at the edges of the torn membrane, where they self-assemble into 2D arrays. The formation of 2D arrays strengthens the damaged sarcolemma, counteracts the tensions exerted by the cortical cytoskeleton and thus prevents the expansion of the tear. We showed also that a pool of endogenous AnxA5 binds to intracellular vesicles that obstruct the wounding site. It is likely these vesicles, once associated one to each other, ensure membrane resealing. Our results suggest that sarcolemma repair of damages caused by PFTs is independent of AnxA5. Therefore, different membrane repair mechanisms may exist, their occurrence probably depending on the type and/or the size of damages. Finally, we performed studies on muscle cells established from patients diagnosed with limb girdle muscular dystrophies type 2B (dysferlin-deficient) and 1C (caveolin-3-deficient), respectively. We found that dysferlin or caveolin-3 deficiency leads to a defect of membrane repair, in the case of mechanical damages. AnxA5 behaved similarly in these damaged cells and wild-type cells, suggesting that its function is independent of dysferlin or caveolin-3. Unlike dysferlin-deficient cells, damages created by PFTs are efficiently repaired in caveolin- 3-deficient cells. This result supports the hypothesis that different mechanisms occur in muscle cells, depending on the type of damage. In conclusion, this work indicates that AnxA5 is a key component of the membrane repair machinery, in the case of mechanical disruptions. Our results enable to propose a detailed mode of action for AnxA5
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Arraud, Nicolas. "Etude cinétique de la liaison élémentaire entre Annexine-A5 et membranes et mise au point d’un test de quantification des microparticules plasmatiques pro-coagulantes, par cytométrie en flux." Thesis, Bordeaux 1, 2011. http://www.theses.fr/2011BOR14459/document.
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L’Annexine A5 (AnxA5) est une protéine soluble se liant aux membranes contenant de la phosphatidylsérine (PS) en présence de calcium (Ca2+). Le rôle central joué par l’AnxA5 dans les processus de réparation membranaire a été récemment mis en évidence. L’AnxA5 possède une très forte affinité pour les membranes biologiques contenant de la PS, cependant son mode de liaison aux membranes n’est pas encore élucidé.La première partie de mon travail de thèse a concerné le développement d’une approche originale d’étude de la liaison de l’AnxA5 à des microsphères de silice fonctionnalisées par une bicouche lipidique (µPSiO2@SLB pour supported lipid bilayer), par cytométrie en flux (FCM). Cette approche m’a permis d’étudier la liaison à l’équilibre et en cinétique à très faible concentration en AnxA5, de l’ordre du picomolaire. Cette approche représente une des méthodes les plus sensibles d’étude de liaison à l’équilibre et la première permettant d’accéder aux constantes cinétiques d’interaction pour l’AnxA5. Cette étude m’a également permis de mettre au point une stratégie de dosage indirect de liposomes contenant de la PS avec une sensibilité de l’ordre du nanogramme de lipides par millilitre.La seconde partie de ma thèse a concerné l’étude de microparticules (MP), fragments de membranes cellulaires présents dans les fluides biologiques. Dans le plasma sanguin la majorité des MP sont d’origine plaquettaire et exposent de la PS. Il existe une corrélation entre la concentration en MP plasmatiques exposant de la PS et le développement de pathologies thrombotiques. La FCM est la méthode de référence dans l’étude des MP cependant leur détection est rendue difficile par leur petite taille. J’ai appliqué aux MP plasmatiques le test de dosage développé pour les liposomes. Les résultats obtenus sont prometteurs et permettent d’envisager le développement d’un test de dosage de l’ensemble des MP exposant de la PSAnnexin-A5 (AnxA5) is a soluble membrane binding protein that binds to phosphatidylserine (PS) containing membranes in a calcium dependent manner and plays a central role in cell membrane repair processes. AnxA5 has a remarkably high affinity for PS containing membranes, but its binding mechanism remains unclear.The first part of my PhD work was to develop a new method for studying AnxA5 binding using supported lipid bilayer functionalized silica microspheres (µPSiO2@SLB) and Flow Cytometry (FCM). This approach allowed me to describe in details both equilibrium and kinetics of AnxA5 binding at picomolar concentrations in AnxA5. This study is one of the most sensitive for equilibrium binding studies and the first allowing to measure binding kinetics constants for AnxA5. This study also led to the development of a new strategy for determination of liposome concentration with sensitivity in the range of one nanogram of lipid per milliliter. The second part of my work focused on microparticles (MP) that are cell membrane fragments found in biological fluids. In plasma, the vast majority of MP originates from platelets and expresses PS at their surface. There is a correlation between MP concentration in plasma and thrombotic risk. FCM is the “golden standard” of hæmatologic analysis but the majority of MPs are too small to be detected. I have applied the test developed with liposomes for the quantification of MP. The results are promising and allow foreseeing the development of a test able to give the absolute quantity of PS exposing MPs in plasma samples
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Cederholm, Anna. "Novel immunological mechanisms and factors in systemic lupus erythematosus-related cardiovascular disease /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-679-4/.
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Petri, Simone Carolina Soares. "Efeitos de derivados nitro heterocíclicos sintéticos sobre formas promastigotas e amastigotas intracelular de Leishmania (Leishmania) infantum." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-26102015-145221/.
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INTRODUÇÃO: A leishmaniose visceral (LV), pertence ao grupo de endemias consideradas prioritárias no mundo. É uma doença grave e com poucas opções de tratamento e, mesmo quando adequadamente tratada, possui um nível de letalidade de 5 a 7%. Apesar da expansão da doença, o tratamento para leishmaniose visceral não obteve avanços. O tratamento da leishmaniose possui apenas dois grupos de medicamentos utilizados: os antimonoiais e os não-antimoniais. Os compostos nitroheterocíclicos foram utilizados pois acredita-se que a eficácia desta classe de compostos está na habilidade desses compostos inibirem a tripanotiona redutase. Os compostos foram obtidos por via sintética e refinados pelo método QSAR por remodelagem molecular. Foram obtidos séries de compostos nitroheterocíclicos, onde a série BSF (derivados 5-nitro-2-furfurilideno - azometínicos) foi utilizada para avaliar a bioatividade in vitro destes compostos frente à Leishmania. Para avaliação da atividade anti-Leishmania foram usadas formas promastigotas de Leishmania (Leishmania) infantum. Os métodos utilizados para determinar a atividade anti-Leishmania dos compostos da série BSF foram os métodos colorimétrico 3-[4,5-dimetiltiazol-2-il] 2,5 brometo de difeniltetrazólio (MTT), apoptose por Anexina V e reação de Griess (dosagem de NO). Ao comparar os resultados com os respectivos controles positivos e com a Anfotericina B, foi observado que a atividade anti-Leishmania em formas promastigotas de L. L. infantum dos compostos foi menos significativa quando comparado com anfotericina B. Porém, ao comparar os resultados de macrófagos infectados e citotoxicidade com a anfotericina B, os compostos mostraram resultados expressivos, ao apresentarem baixa taxa de citotoxicidade e significativa diminuição da proliferação intracelular. A expressiva produção de nitrito pelos macrófagos infectados tratados com os compostos da série BSF sugere-se que estes compostos possuam uma ação indireta de potencialização de produção de NO nas células hospedeiras. Os resultados in vitro utilizando derivados nitroheterocíclicos mostraram atividade destes sobre formas promastigotas e amastigotas intracelulares, e são compostos em potencial para avaliação de efeito in vivo contra leishmaniose visceralINTRODUCTION: Visceral leishmaniasis (VL) belongs to the group of endemics prioritized worldwide. It is a serious disease with few treatment options, and even when adequately treated, it has a lethality level of 5 to 7%. Despite the expansion of the disease, treatment for visceral leishmaniasis has not made progress. Treatment of leishmaniasis has used only two groups of drugs: antimonial and non-antimonial. Nitro-heterocyclic compounds were used in this study because it is believed that the effectiveness of this class of compounds is the ability to inhibit trypanothione reductase. The compounds were obtained synthetically and refined by QSAR method molecular remodeling. Nitro-heterocyclic series of compounds were obtained, where the BSF series (derived from 5-nitro-2-furfurylidene - azometínicos) was used to evaluate the in vitro bioactivity of these compounds against the Leishmania. To evaluate the anti-Leishmania activity, promastigotes of Leishmania (Leishmania) infantum were used. The methods used to determine the anti-Leishmania activity of the BSF series compounds were colorimetric methods 3-[4,5-dimethylthiazol-2-yl] 2,5-diphenyltetrazolium bromide (MTT), apoptosis by Annexin V, and Griess reaction (IN dosage). By comparing the results with the respective positive controls and with amphotericin B, it was observed that the anti-Leishmania activity of L. L. infantum promastigotes of the compounds was less significant when compared with amphotericin B. However, comparing the results of infected macrophages and cytotoxicity with amphotericin B, compounds showed significant results, presenting low cytotoxicity rate and significant decrease in intracellular proliferation. The significant nitrite production by infected macrophages treated with the BSF series compounds suggested that these compounds have an indirect potentiation action in the NO production in the host cells. In vitro results using nitro-heterocyclic derivatives showed their activity on these promastigotes and intracellular amastigotes, and presented them as potential compounds for in vivo effect evaluation against visceral leishmaniasis
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Wehder, Liane [Verfasser], Ferdinand von [Akademischer Betreuer] Eggeling, Stephan [Akademischer Betreuer] Diekmann, and Jens [Akademischer Betreuer] Habermann. "Molekulares Imaging (MALDI-IMS) humaner Kopf-Hals-Tumore und funktionelle Analyse pathologisch exprimierter Proteine am Beispiel von S100A8 und Annexin A5 / Liane Wehder. Gutachter: Ferdinand von Eggeling ; Stephan Diekmann ; Jens Habermann." Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2014. http://d-nb.info/1046563386/34.
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Linares, Romain. "Caractérisation, quantification et isolation de vésicules extracellulaires du plasma sanguin à l’aide de nanoparticules d’or ou magnétiques conjuguées à des protéines." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0344/document.
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Les vésicules extracellulaires (VEs) sont des vésicules membranaires de taille majoritairement submicrométrique présentes dans les fluides biologiques et émises par les cellules en réponse à divers stimuli. Les VEs sont impliquées dans de nombreux phénomènes physiologiques mais également dans des pathologies telles que cancers ou maladies cardiovasculaires. Elles pourraient donc être utilisées comme biomarqueurs de ces pathologies. Bien que les VEs soient aujourd’hui largement étudiées, nos connaissances sur le sujet demeurent limitées. Ceci est principalement dû aux difficultés de caractérisation des VEs et à l’absence de standardisation de leurs méthodes d’étude et d’isolation. La première partie de mon travail de thèse a porté sur le développement d’une méthode de thiolation de protéines. Des anticorps ont été modifiés pour exposer des thiols et ont été conjugués à des nanoparticules d’or fonctionnalisées par des maléimides. Le couplage des anticorps thiolés aux nanoparticules d’or a été étudié de manière quantitative et des conditions de conjugaison optimales ont été déterminées par des approches biochimiques. La seconde partie de ce travail a concerné la caractérisation des VEs du plasma sanguin de sujets sains par microscopie électronique à transmission (MET). La morphologie, la taille et le phénotype des VEs ont été déterminés par cryo- MET combinée au marquage par des nanoparticules d’or conjuguées à des protéines. La quantification objective des VEs du plasma sanguin a été réalisée à l’aide d’une méthode originale de MET basée sur la sédimentation de VEs sur grille de MET. La troisième partie de cette étude a consisté à mettre au point une méthode d’isolation de VEs à l’aide de particules magnétiques conjuguées à de l’AnxA5. Des conditions permettant d’extraire la totalité des VEs exposant la phosphatidylsérine contenues dans un plasma sanguin ont été déterminées par cytométrie en flux (CF). Ce travail a permis d’apporter une caractérisation détaillée des VEs du plasma sanguin du sujet sain et peut servir de référence pour des études ultérieures concernant les VEs contenues dans des plasmas ou autres liquides biologiques pathologiquesExtracellular vesicles (EVs) are submicrometric membrane vesicles found in body fluids and produced by cells in response to various stimuli. EVs are involved in numerous physiological processes but also in pathologies as cancers or cardiovascular diseases. Even if EVs are largely studied, our knowledge about them remains limited. This is mainly caused by the difficulties to characterize EVs and by the lack of standardized methods allowing their characterization. The first part of my PhD work focused on the development and optimization of a protein thiolation method. Antibodies modified to expose few thiols were conjugated to gold nanoparticles functionalized with maleimides. The binding of thiolated antibodies to gold nanoparticles was quantitatively studied and optimal conjugation conditions were determined using biochemical methods. The second part of my PhD work concerned the characterization of blood plasma EVs from healthy subjects using transmission electron microscopy (TEM). EVs morphology, size and phenotype were determined by cryo-TEM combined with labelling with protein-conjugated gold nanoparticles. The near-absolute quantification of blood plasma EVs was achieved using an original TEM method based on the direct sedimentation of EVs onto TEM grids. The third part of this study consisted in developing an EV isolation method using AnxA5-conjugated magnetic particles. Conditions allowing total extraction of blood plasma phosphatidylserine-exposing EVs were determined using flow cytometry (FC). This study presents a detailed characterization of blood plasma EVs from healthy subjects and can serve as a reference for future studies on EVs contained in pathological plasmas or other body fluids
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Figge, Lena. "Synthese molekularer Bildgebungssonden für die molekulare Magnetresonanztomographie." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät, 2014. http://dx.doi.org/10.18452/16992.
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Zweck der molekularen Bildgebung ist es, biologische Prozesse auf zellulärer und molekularer Ebene zu messen und zu charakterisieren, um so die Ursachen von Krankheiten und Veränderungen im Organismus zu diagnostizieren. Sie basiert auf dem Einsatz molekularer Bildgebungssonden, welche einen spezifischen biologischen Vorgang darstellen oder sich spezifisch in dem zu untersuchenden Gewebe anreichern oder aktiviert werden. Ziel dieser Arbeit war die Entwicklung und Analyse neuer Bildgebungssonden für die spezifische in-vivo-Bildgebung der Apoptose und von Enzymaktivitäten mittels Magnetresonanztomographie (MRT) auf der Grundlage sehr kleiner Eisenoxidnanopartikel (very small iron oxide particles, VSOP). VSOP sind superparamagnetisch und durch ihre negativ geladene Citrathülle elektrostatisch stabilisiert. Für die Apoptose-Bildgebung sollte durch Bindung des Proteins Annexin A5 (AnxA5) an die Citrathülle der VSOP eine zielgerichtete Sonde hergestellt werden (AnxA5-VSOP). Für die Bildgebung von Enzymaktivitäten sollte eine durch die Matrixmetalloproteinase-9 (MMP-9) aktivierbare Sonde hergestellt werden (Protease-spezifische Eisenoxidpartikel, PSOP).The goal of molecular imaging is to characterize and measure biological processes at cellular and molecular levels for the purpose of diagnosing the cause of diseases and molecular abnormalities. Molecular imaging is based on the use of probes with a high affinity to the target tissue and / or which are specifically activated. The aim of this study was to develop and analyze new molecular imaging probes for the in vivo imaging of apoptosis and enzyme activity using magnetic resonance imaging (MRI), based on very small iron oxide particles (VSOP). VSOP are superparamagnetic and electrostatically stabilized due to their negatively charged citrate surface. For the imaging of apoptosis the protein annexin A5 (AnxA5) was coupled to the citrate surface (AnxA5-VSOP). For the imaging of enzyme activities an activatable imaging probe with a cleavage site for the matrix metalloproteinase 9 (MMP-9) was synthesized (protease-specific iron oxide particles, PSOP).
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Bérat, Rémi. "Assemblages 2D de l'Annexine A5 : applications biotechnologiques & aspects fonctionnels." Bordeaux 1, 2007. http://www.theses.fr/2007BOR13495.
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L'Annexine A5 (Anx5) est une protéine de la famille des annexines qui présente la propriété de s'organiser à la surface des bicouches lipidiques en trimères et en assemblages bidimensionnels (2D) de trimères. Ce travail de thèse concerne le développement d'applications biotechnologiques des assemblages 2D d'Anx5 ainsi qu'une étude des propriétés fonctionnelles de ces assemblages. Ces travaux ont été réalisés principalement à l'aide des méthodes de la microbalance à cristal de quartz avec mesure de dissipation (QCM-D) et de la microscopie à force atomique (AFM). La première partie de cette thèse concerne le développement de plates-formes d'ancrage basées sur des assemblages 2D de protéines dérivées de l'Anx5. Des complexes covalents entre l'Anx5 et des peptides d'adhésion cellulaire pour la réalisation de plates-formes d'ancrage de cellules. Des protéines de fusion entre l'Anx5 et un fragment de la protéine A ont d'autre part servi au développement de plates-formes 2D pour l'immobilisation contrôlée d'anticorps et de protéines. La seconde partie de cette thèse concerne l'étude des propriétés fonctionnelles des assemblages 2D d'Anx5. L'étude de l'interaction d'un anticorps anti-phospholipide avec les assemblages 2D d'Anx5 montre que cet anticorps ne perturbe pas l'organisation 2D de l'Anx5. La seconde étude concernant l'influence des assemblages 2D de l'Anx5 sur la dynamique des bicouches lipidiques établie une corrélation entre la formation de trimères et le ralentissement de la dynamique des membranes. Ces travaux contribuent à notre compréhension des propriétés des assemblages 2D d'Anx5 et permettent d'envisager le développement de biocapteurs pour cellules ou molécules.
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Le, Drévo Marie-Anne. "L'Annexine A5 : une nouvelle protéine régulatrice du canal CFTR (cystic fibrosis transmembrane conductance regulator)." Brest, 2007. http://www.theses.fr/2007BRES3201.
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Le cystic fibrosis transmembrane conductance regulator (CFTR) est un canal chlorure cAMPdependant dont la fonction peut-être régulée par des interactions protéine-protéines. Cependant, on connaît encore mal l’étendue et l’importance de ces intéractions. Sachant que I’ annexine A5 (anxA5) est surexprimée dans la mucoviscidose et que l’anxA5 et le CFTR partagent certaines propriétés, nous avons émis l’hypothèse selon laquelle ces deux protéines interagissent physiquement et/ou fonctionnellement. Dans la première partie de cette thèse, nous montrons pour la première fois que l’anxA5 se lie au domaine NBD1 (nucleotide-binding domain 1) du CFTR et que cette interaction est renforcée en présence de Ca2+ et d’ATP. Nous montrons également que la diminution de l’expression de l’anxA5 est corrélée avec une diminution de la fonction du canal CFTR. Nous concluons donc que l’anxA5 est nécessaire au fonctionnement normal du CFTR. Dans une seconde partie, nos résultats indiquent que la surexpression de l’anxA5 permet de corriger partiellement le défaut d’expression du canal CFTR dans la membrane plasmique induit par la mutation ΔF508, la mutation la plus fréquente. De plus, nous montrons que l’augmentation de la concentration intracytosolique en Ca2+, induite par la thapsigargine, permet de potentialiser l’effet de I ‘anxA5. L’ensemble de ces résultats suggère que l’anxA5 peut être envisagée comme une cible thérapeutique potentielleThe cystic fibrosis transmembrane conductance regulator (CFTR) functions as a cAMP-activated chloride channel which is regulated by protein-protein interactions. The extent to which CFTR is regulated by these interactions remains unknown. Annexin A5 (anxA5) is overexpressed in cystic fibrosis (CF) and given the functional properties of anxA5 and CFTR we considered whether they are associated and if so whether this has implications for CFTR function. In the first part of this thesis, we show for the first time that anxA5 is associated with nucleotide-binding domain 1 (NBD1) of CFTR and that this interaction is Ca2+ and ATP-dependent. The decreased anxA5 expression was correlated with a decreased CFTR chloride channel function. We concluded that anxA5 is necessary for normal CFTR chloride channel activity. In the second part of this thesis, our results indicated that the overexpression of anxA5 permitted to partially correct the ceIl surface expression defect of the misfolded ΔF508-CFTR, the most common mutation. Moreover, we show that the increase of intracytosolic Ca2+ concentration, induced by a thapsigargin treatment, allowed to increase the anxA5 effect. All these results suggest that anxA5 may be seen as a potential therapeutic target
Book chapters on the topic "Annexin A5"
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Stöcker, W. "Autoantikörper gegen Annexin A5." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_350-1.
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Stöcker, W. "Autoantikörper gegen Annexin A5." In Springer Reference Medizin, 246–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_350.
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Govorukhina, Natalia, Wilma Bergsma-Schutter, Christine Mazères-Dubut, Serge Mazères, Eugenia Drakopoulou, Leonid Bystrykh, Frank Oling, et al. "Self-Assembly of Annexin A5 on Lipid Membranes." In Annexins, 61–78. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9214-7_4.
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Du, Xuezhong, David W. Britt, and Vladimir Hlady. "Annexin A5 Binding and Rebinding to Mixed Phospholipid Monolayers Studied by SPR and AFM." In ACS Symposium Series, 419–32. Washington, DC: American Chemical Society, 2012. http://dx.doi.org/10.1021/bk-2012-1120.ch019.
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Zhao, Yan, Yuji Kuge, Songji Zhao, H. William Strauss, Francis G. Blankenberg, and Nagara Tamaki. "Molecular Imaging of Atherosclerotic Plaque Vulnerability: Comparison between 18F-FDG and 99mTc-Annexin A5." In Molecular Imaging for Integrated Medical Therapy and Drug Development, 69–77. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-98074-2_8.
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"Annexin-A5-Antikörper." In Springer Reference Medizin, 136. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_310181.
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"Anti-Annexin-A5-Antikörper." In Springer Reference Medizin, 138. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_300106.
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"Annex A5." In Learning Mathematics for Life, 241–44. OECD, 2010. http://dx.doi.org/10.1787/9789264075009-14-en.
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"Annexe A5 Compléments sur la projection stéréographique." In Symétrie et propriétés physiques des cristaux, 107–12. EDP Sciences, 2020. http://dx.doi.org/10.1051/978-2-7598-0927-1-011.
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"Annexe A5 Compléments sur la projection stéréographique." In Symétrie et propriétés physiques des cristaux, 107–12. EDP Sciences, 2020. http://dx.doi.org/10.1051/978-2-7598-0927-1.c011.
Full textConference papers on the topic "Annexin A5"
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Rogenhofer, N., A. Markoff, X. Ennerst, N. Bogdanova, and CJ Thaler. "Maternale sowie paternale M2/Annexin-A5 Trägerschaft als Risikofaktor für rezidivierendes Implntationsversagen (RIF)." In Kongressabstracts zur Tagung 2020 der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe (DGGG). © 2020. Thieme. All rights reserved., 2020. http://dx.doi.org/10.1055/s-0040-1717691.
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