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Artykuły w czasopismach na temat "Récepteurs de la thrombine"
Jandrot-Perrus, Martine. "La thrombine et ses récepteurs : implications dans l’hémostase et le développement embryonnaire". médecine/sciences 18, nr 1 (styczeń 2002): 19–22. http://dx.doi.org/10.1051/medsci/200218119.
Pełny tekst źródłaVanObberghen-Schilling, E., i J. Pouysségur. "Le récepteur de la thrombine et ses implications dans la prolifération des cellules vasculaires". médecine/sciences 9, nr 10 (1993): 1043. http://dx.doi.org/10.4267/10608/2807.
Pełny tekst źródłaRullier, A., J. Gillibert-Duplantier, G. Cubel, M. Capdepont, N. Senant, C. Petibois, P. Costet i J. Rosenbaum. "CO 13-L’invalidation du gène du protease-activated receptor 1, le principal récepteur de la thrombine, protège de la fibrose hépatique". Gastroentérologie Clinique et Biologique 30, nr 8-9 (sierpień 2006): 1040. http://dx.doi.org/10.1016/s0399-8320(06)73392-9.
Pełny tekst źródłaBoutière-Albanèse, Brigitte. "Temps de thrombine". EMC - Biologie Médicale 1, nr 1 (styczeń 2006): 1–4. http://dx.doi.org/10.1016/s2211-9698(06)76183-0.
Pełny tekst źródłaA., F. "Inhibiteur de la thrombine". Médecine des Maladies Métaboliques 3, nr 6 (grudzień 2009): 614. http://dx.doi.org/10.1016/s1957-2557(09)73631-4.
Pełny tekst źródłaHorellou, Marie-Hélè;ne, Jacqueline Conard i Michel Samama. "Allongement du temps de thrombine". EMC - Traité de médecine AKOS 1, nr 1 (styczeń 2006): 1–2. http://dx.doi.org/10.1016/s1634-6939(06)75179-1.
Pełny tekst źródłaManus, Jean-Marie. "D’une anti-thrombine à l’autre". Revue Francophone des Laboratoires 2009, nr 412 (maj 2009): 13. http://dx.doi.org/10.1016/s1773-035x(09)73913-9.
Pełny tekst źródłaPrati, Clément, Evelyne Racadot, Jean-Pierre Cédoz, Éric Toussirot i Daniel Wendling. "Polyarthrite rhumatoïde et génération de thrombine". Revue du Rhumatisme 79, nr 6 (grudzień 2012): 575–76. http://dx.doi.org/10.1016/j.rhum.2012.03.011.
Pełny tekst źródłaLetonturier, Philippe. "Un inhibiteur de thrombine appelé ximélagatran". La Presse Médicale 34, nr 5 (marzec 2005): 402. http://dx.doi.org/10.1016/s0755-4982(05)83930-2.
Pełny tekst źródłaEspitia, O., i M. Fouassier. "Le test de génération de thrombine". La Revue de Médecine Interne 36, nr 10 (październik 2015): 690–93. http://dx.doi.org/10.1016/j.revmed.2015.04.013.
Pełny tekst źródłaRozprawy doktorskie na temat "Récepteurs de la thrombine"
Faraut, Brice. "Synaptogénèse et plasticité neuromusculaire : conséquences de l'activation du récepteur de la thrombine, PAR-1". Paris 5, 2004. http://www.theses.fr/2004PA05P612.
Pełny tekst źródłaThrombin is a serine protease that regulates numerous cellular functions by activating via specific proteolytic cleavage a family of G-protein-coupled receptors (PARs). The thrombin receptor PAR-1 and the thrombin inhibitor protease nexin-1 are both expressed by muscle cells during the formation of the neuromuscular junction (NMJ). We have then hypothesized that thrombin was involved in the formation and plasticity of the NMJ. We show in myotubes in vitro that thrombin, by activating PAR-1, decreases the expression of the acetylcholine receptor (AChR) while its specific inhibitor, hirudin, increases its expression. In addition, this effect of thrombin is mediated through intracellular calcium signals IP3 receptor-dependent. Then, in neuron-myotube cocultures, we show that thrombin via PAR-1 decreases neuromuscular contact size whereas hirudin has the opposite effect. Therefore, we have studied the expression of the muscle-specific tyrosine-kinase receptor, MuSK, which activation leads to the aggregation of AChRs mediated by rapsyn and of other post-synaptic proteins during the formation of neuromuscular contacts. We find that rapsyn expression is not changed but the one of MuSK is reduced in presence of thrombin. In conclusion, this study reveals a signaling pathway for AChR regulation by thrombin and significant modifications of neuromuscular synaptogenesis when MuSK and AChR levels are reduced by thrombin. Recently, mutations in MuSK gene have been identified by our team for the first time in neuromuscular human pathology. To study the pathogen features of these mutations, this latter have been expressed in muscle cells and the repercussion on neuromuscular synaptogenesis were analysed in vitro. We find that a nonsense mutation of the intracellular domain of MuSK decreases AChR e-subunit gene transcription and also induces an exuberant axonal growth in neuron-myotube cocultures. All together, this data contribute to a better comprehension of the mechanisms involved in the formation and the maintenance of the NMJ
Zolotoff, Cindy. "Effets combinés de l'hypoxie intermittente et de la thrombine sur un modèle in vitro de Barrière Hémato-Encéphalique". Electronic Thesis or Diss., Lyon, 2021. http://www.theses.fr/2021LYSES020.
Pełny tekst źródłaObstructive sleep apnea (OSA) is characterized by decreases or cessation of airflow followed by periods of reoxygenation. Several studies suggest a link with the onset of neurodegenerative diseases that could be due to an alteration of the blood-brain barrier (BBB), an interface that protects the brain from potential harmful compounds. This interface is made up of endothelial cells connected by junctional proteins that limit passage, and they also possess efflux pumps that play a role in detoxifying molecules. Repeated episodes of intermittent hypoxia (IH) would be at the origin of the alteration of this BBB. Other factors could be involved since OSA also increases the incidence of vascular pathologies and thrombin, a coagulation protease acting through its PAR receptors, could be increased. We therefore developed a cellular model of IH which allowed us to see that IH induced: a disruption of the BBB marked by a decrease in the expression of junction proteins, an increase in permeability and a deregulation of efflux pumps. Next, we combined IH and thrombin at two concentrations. IH alone or combined with a high dose of thrombin increases BBB permeability and PAR-1 expression, an effect that can be reversed by the use of dabigatran. IH combined with a lower dose of thrombin limits BBB permeability and increases PAR-3 expression. Thus, this work has allowed a first approach of the cellular mechanisms taking place in OSA
Saci, Abdelhafid. "Etude de la signalisation plaquettaire : implication de p120Cbl, phosphatidylinositol 3-kinase (PI 3-K) et Grb2". Paris 5, 2001. http://www.theses.fr/2001PA05P605.
Pełny tekst źródłaBlood platelets are anucleated and terminaly differenciated cells. A number of receptors are present on platelet membrane and mediate signalling and activation in response to various agonists. The action of an agonist triggers an inside-out signalling which activates αIIb-β3 integrin. The latter becomes able to link fibrinogen and transduces a secondary outside-in signalling. We first studied the involvement of the adoptor protein, Cbl, and of the lipid kinase, PI 3-K, in platelet signalling mediated by (i) the receptor for Fc domain of IgG (FcγRIIa), (ii) by the αIIb-β3 integrin (outside-in) and (iii) by the thrombin receptor. .
Jumeau, Céline. "La thrombine et son récepteur PAR-1 comme cibles thérapeutiques dans la prévention et le traitement de la dilatation atriale". Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066242.
Pełny tekst źródłaAtrial fibrillation (AF) is the most common cardiac arrhythmia. It is characterized by a disorganized and ineffective contraction of the atria and structural changes of the myocardium. Endothelial dysfunction, maintained by inflammation, activate the coagulation cascade and thrombin generation, promoting intra-atrial thrombus formation. Prevention of thromboembolism is a major issue in the management of AF and is done by long-term prescription of oral anticoagulants among which a direct thrombin inhibitor, dabigatran. Our hypothesis is that excess thrombin maintains structural changes in the myocardium via the PAR-1 receptor (protease activated receptor-1) of circulating and myocardial cells. The objective is to identify the signaling pathway of thrombin involved in the atrial remodeling. In an atrial dilatation model associated with arrhythmogenic substrate and hypercoagulability, administration of direct thrombin inhibitors or antagonists of PAR-1 oral reduce expansion and arrhythmic susceptibility of the left atrium. These treatments inhibit the induction of myocyte hypertrophic response markers, β-MHC and BNP and remodeling of the extracellular matrix markers, CTGF and PAI-1. With explant of left atria culture, we show that these phenotypic changes are induced by the Rho pathway / ROCK and STAT3 transcription factor. Our results also indicate that the expression and activity of ErbBs receptors known to be transactivated via PAR-1, are modified during development of atrial dilatation. Thrombin participates in these changes only when the atrial remodeling is established. These results show that thrombin participates in atrial remodeling associated with an arrhythmogenic substrate, and direct thrombin inhibitors and PAR-1 antagonists are potential therapeutic agents to prevent the development of atrial dilation
Li, Ruo Ya. "Clonage d'une tyrosine-phosphatase membranaire (HPTP-béta) et étude de l'implication de la SH-PTP1 dans l'agrégation plaquettaire induite par la thrombine". Toulouse 3, 1995. http://www.theses.fr/1995TOU30150.
Pełny tekst źródłaGaits-Iacovoni, Frédérique. "Intervention de protéine tyrosine phosphatases dans l'inhibition de contact des cellules endothéliales et dans l'activation de cellules mégacaryoblastiques". Toulouse 3, 1995. http://www.theses.fr/1995TOU30245.
Pełny tekst źródłaGuinebault, Christine. "Activation plaquettaire par l'alpha-thrombine : modes de régulation de la phosphatidylinositol 3-kinase et de la phospholipase C-gamma, en relation avec l'organisation du cytosquelette". Toulouse 3, 1994. http://www.theses.fr/1994TOU30261.
Pełny tekst źródłaMokrane, Ahmed. "Modélisation de la réactivité enzymatique par le formalisme LSCF et étude des effets électrostatiques à longue distance : application à l'activation du récepteur de la thrombine". Nancy 1, 1997. http://docnum.univ-lorraine.fr/public/SCD_T_1997_0272_MOKRANE.pdf.
Pełny tekst źródłaDufourcq, Pascale. "La thrombomoduline, un marqueur de la lésion endothéliale : approche clinique et expérimentale dans la maladie athéromateuse". Bordeaux 2, 1994. http://www.theses.fr/1994BOR2P019.
Pełny tekst źródłaSmadja, David. "Rôle du récepteur de la thrombine PAR-1 dans l'expansion des progéniteurs endothéliaux". Paris 5, 2006. http://www.theses.fr/2006PA05P625.
Pełny tekst źródłaThe injection of endothelial progenitor cells (EPCs) in preclinical models of ischemia has been shown to enhance neovascularization. However, the scarcity of EPCs in human peripheral blood is a limitation for of its use as a cell therapy product, and the development of an expansion procedure is a crucial issue. In this work, we have characterized EPCs during in vitro expansion, using EPCs derived from cord blood CD34+ cells. An increased expression of KDR/VEGFR2 along expansion was observed, together with an increase of in vitro angiogenic properties. We also show the presence of the thrombin receptor PAR-1 on expanded EPCs. The importance of PAR-1 in blood vessel development has been demonstrated in knockout mice. As EPCs are thought to be involved in postnatal vasculogenesis, we examined the effect of PAR-1 activation on EPCs. PAR-1 activation induced EPCs proliferation, resulting of an angiopoietin 2 upregulation. PAR-1 activation also enhanced actin reorganization, promoting both spontaneous migration in a Boyden chamber assay and migration toward SDF-1. Finally, PAR-1 stimulation by SFLLRN increased the formation of capillary-like structures formed by EPCs in Matrigel, and this effect was abrogated by anti-CXCR-4 and anti-SDF-1 antibodies. All together, PAR-1 activation on cord blood derived EPCs led to a proangiogenic effect. In vivo, enhancement of angiogenic properties of EPCs by thrombin generated at the target site might promote vasculogenesis and thrombus resorption. Our data suggest that SFLLRN peptide could be used to expand cord blood derived-EPCs ex vivo. However, this effect was not found on EPCs isolated from adult blood, underlining the usefulness of a procedure designed to mobilize immature endothelial cells from bone marrow to peripheral blood
Książki na temat "Récepteurs de la thrombine"
Advances in adrenergic receptor biology. Amsterdam: Elsevier, 2011.
Znajdź pełny tekst źródła(Firm), Knovel, red. Microwave receivers with electronic warfare applications. Wyd. 2. Raleigh, N.C: Scitech Pub., 2005.
Znajdź pełny tekst źródłaEisenson, Henry L. Scanners & secret frequencies. San Diego: Index Pub. Group, 1993.
Znajdź pełny tekst źródłaR, Ruffolo Robert, i Hollinger Mannfred A, red. G-protein coupled transmembrane signaling mechanisms. Boca Raton, Fla: CRC Press, 1995.
Znajdź pełny tekst źródłaM, Gotto Antonio, O'Malley Bert W i Fondation Princesse Liliane, red. The role of receptors in biology and medicine: Proceedings of the Ninth Argenteuil Symposium. New York: Raven Press, 1986.
Znajdź pełny tekst źródłaSpampinato, Santi M. Opioid receptors: Methods and protocols. New York: Humana Press, 2015.
Znajdź pełny tekst źródłaE, Giesen-Crouse, red. Peripheral benzodiazepine receptors. London: Academic Press, 1993.
Znajdź pełny tekst źródła1936-, Kalsner Stanley, Westfall Thomas C i New York Academy of Sciences., red. Presynaptic receptors and the question of autoregulation of neurotransmitter release. New York, N.Y: New York Academy of Sciences, 1990.
Znajdź pełny tekst źródłaJacques, Bertoglio, Fradelizi Didier i Institut national de la santé et de la recherche médicale (France), red. Lymphokine receptor interactions =: Interactions lymphokines-récepteurs : proceedings of the VIth International Lymphokine Workshop held in Evian (France), October 23-27, 1988. Paris: INSERM, 1989.
Znajdź pełny tekst źródłaLipsky, Stephen E. Microwave passive direction finding. New York: Wiley, 1987.
Znajdź pełny tekst źródłaCzęści książek na temat "Récepteurs de la thrombine"
Robert, Jacques. "Les voies des récepteurs lymphocytaires". W Signalisation cellulaire et cancer, 155–62. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_14.
Pełny tekst źródłaRobert, Jacques. "Les voies des récepteurs nucléaires". W Signalisation cellulaire et cancer, 163–75. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_15.
Pełny tekst źródłaRobert, Jacques. "Récepteurs couplés à des canaux ioniques". W Signalisation cellulaire et cancer, 177–87. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_16.
Pełny tekst źródłaLoriot, Y., i B. Besse. "Molécules inhibitrices des récepteurs du VEGF". W Les thérapies ciblées, 65–78. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-36008-4_5.
Pełny tekst źródłaRobert, Jacques. "Les voies des récepteurs couplés aux protéines G". W Signalisation cellulaire et cancer, 91–102. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_7.
Pełny tekst źródłaRobert, Jacques. "Les récepteurs toll-like, l’interleukine 1 et le NFκB". W Signalisation cellulaire et cancer, 145–54. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_13.
Pełny tekst źródłaRobert, Jacques. "Les facteurs de croissance et les récepteurs à activité tyrosine kinase". W Signalisation cellulaire et cancer, 21–43. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_2.
Pełny tekst źródłaBedel, R., C. Borg i P. Saas. "CTLA-4 et Toll-like récepteurs: de nouvelles cibles en immunothérapie". W Les thérapies ciblées, 169–95. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-36008-4_12.
Pełny tekst źródłaHammar, K., S. Moulessehoul, A. Tou, F. Kemas, H. Benamar i M. Ghalek. "Ciblage des récepteurs ErbB (HER) chez 45 patientes atteintes de cancer du sein". W Cancer du sein : surdiagnostic, surtraitement, 247. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0249-7_54.
Pełny tekst źródłaFayette, J., B. Fleury i J. Y. Blay. "Nouvelles approches dans les thérapeutiques ciblées: les récepteurs des facteurs de croissance de type insuline (IGF) et les cyclines". W Les thérapies ciblées, 157–68. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-36008-4_11.
Pełny tekst źródłaStreszczenia konferencji na temat "Récepteurs de la thrombine"
Lim, Chae Young, Eunpyo Choi, Youngkyu Park i Jungyul Park. "3D photonic crystal-based biosensor functionalized with quantum dot-based aptamer for thrombine detection". W SPIE Photonics Europe, redaktorzy Sergei G. Romanov, Gabriel Lozano, Dario Gerace, Christelle Monat i Hernán R. Míguez. SPIE, 2014. http://dx.doi.org/10.1117/12.2054149.
Pełny tekst źródłaVerbeet, M. Ph, R. F. Evers, A. Leyte, H. L. Lamain, A. J. J. Van Ooyen, J. A. Van Mourik i H. Pannekoek. "DETERMINATION OF THE DOMAINS OF FACTOR VIII ESSENTIAL FOR PROCOAGULANT ACTIVITY". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643613.
Pełny tekst źródłaGellee, T., i B. Philippe. "Utilisation combinée des biomatériaux xénogéniques et d’os autologue en chirurgie reconstructrice préimplantaire : Réflexions à propos de quatre indications méconnues". W 66ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206602008.
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