Auswahl der wissenschaftlichen Literatur zum Thema „Transporteurs lipidiques“
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Zeitschriftenartikel zum Thema "Transporteurs lipidiques"
Subra, C., D. Grand, K. Laulagnier, A. Stella, G. Lambeau, M. Paillasse, P. De Medina et al. „R44: Médiateurs lipidiques et cancer : les exosomes comme « signalosomes » intercellulaires transporteurs de prostaglandines“. Bulletin du Cancer 97, Nr. 4 (Oktober 2010): S32—S33. http://dx.doi.org/10.1016/s0007-4551(15)30961-9.
Der volle Inhalt der QuellePelletier, Émilien, und Peter G. C. Campbell. „L’écotoxicologie aquatique - comparaison entre les micropolluants organiques et les métaux : constats actuels et défis pour l’avenir“. Revue des sciences de l'eau 21, Nr. 2 (22.07.2008): 173–97. http://dx.doi.org/10.7202/018465ar.
Der volle Inhalt der QuelleDieng, Sidy Mouhamed, Ahmedou Bamba Kouemel Fall, Nicolas Anton, Patrick Bouriat, Oumar Thioune, Papa Mady Sy, Nadia Massaddeq, Moussa Diop, Mounibé Diarra und Thierry Vandamme. „Emulsions de Pickering stabilisées par des Nanoparticules Solides Lipidiques : Taux de couverture et comportement interfacial“. Journal Africain de Technologie Pharmaceutique et Biopharmacie (JATPB) 2, Nr. 3 (20.12.2023). http://dx.doi.org/10.57220/jatpb.v2i3.117.
Der volle Inhalt der QuelleDissertationen zum Thema "Transporteurs lipidiques"
Basante-Bedoya, Miguel Angel. „Transporteurs lipidiques dans la morphogenèse du champignon pathogène opportuniste de l’Homme Candida albicans“. Electronic Thesis or Diss., Université Côte d'Azur, 2021. http://theses.univ-cotedazur.fr/2021COAZ6030.
Der volle Inhalt der QuelleCandida albicans is a human opportunistic fungal pathogen that can cause superficial or systemic infections; its ability to change from an ovoid to a filamentous form is associated with its virulence. During this highly polarized filamentous growth, an accumulation of vesicles (Spitzenkörper), characteristic of filamentous fungi, as well as a polarized distribution of lipids, such as ergosterol, phosphorylated derivatives of phosphatidylinositol (PI(4)P, PI(4,5)P2) and phosphatidylserine (PS) is observed at the apex of filaments. However, the importance of the asymmetry of these lipids in the membrane bilayer is not completely understood. Flippases (P4-ATPases) transport lipids across the membrane bilayer to generate and maintain its asymmetry. C. albicans has 5 flippases, including Drs2 which is critical for filamentous growth and phosphatidylserine (PS) distribution. Furthermore, a drs2 deletion mutant is hypersensitive to fluconazole and copper. We show here that such a mutant is also critical to virulence in a mouse model of systemic infection. To clarify the role of Drs2 during C. albicans filamentous growth, we studied the distribution of this ATPase, as well as that of key lipids and regulators, during the initiation and maintenance of this growth process. We also characterized point mutants of Drs2, analogous to those altered for PS transport in S. cerevisiae. In addition, we examined the importance of other flippases, such as Dnf1-3, in invasive growth and the role of lipid transporters belonging to the oxysterol binding protein (Osh) family. Our results indicate in particular that Drs2 plays a unique role in the maintenance of invasive filamentous growth of C. albicans, which appears to be more critical after the first septum formation, and that an interaction between Drs2 and Osh4, via PI(4)P, plays an essential role during invasive filamentous growth
Chantemargue, Benjamin. „In silico investigation of xenobiotic interactions with lipid bilayers and ABC membrane transporters, the case of ABCC4/MRP4“. Thesis, Limoges, 2018. http://www.theses.fr/2018LIMO0077/document.
Der volle Inhalt der QuelleUnderstanding the biological mechanisms of action of membrane proteins requires the comprehension of the interactions of xenobiotics with these proteins and with lipid membranes. Experimental methods are often demanding and only partially respond to xenobiotic-membrane-protein interactions. In silico molecular modeling is a serious alternative to tackle these issues. Molecular dynamics (MD) and biased dynamics simulations have opened many perspectives by providing an atomistic description of these intermolecular interactions. Using MD simulations, we built a model of the human ABC ABCC4/MRP4 transporter. We explored the influence of cholesterol on this protein as well as the impact of a polymorphism known to shut down the transport activity of this protein. We also studied the interaction of xenobiotics with this human transporter. The transport cycle of the ABC transporters was investigated in an attempt to better understand how it works.Interactions between lipid membranes and xenobiotics were explored by examining their ability to incorporate lipid membranes. Lipid mixtures with cholesterol showed a significant impact on the human protein ABCC4/MRP4 and on the xenobiotics studied. The importance of regions, domains constituting the ABCC4/MRP4 protein as well as the importance of specific residues has been clearly demonstrated. We also observed intermediates in the transport cycle of an ABC transporter in conjunction with structural changes occurring during this cycle
Ramadan, Alyaa Adel. „Etude de systèmes lipidiques de délivrance de principes actifs“. Phd thesis, Université d'Angers, 2010. http://tel.archives-ouvertes.fr/tel-00586347.
Der volle Inhalt der QuelleOlivier, Maryline. „Rôle du transporteur ABCG1 dans l’homéostasie lipidique cellulaire : implications physiopathologiques chez l'homme“. Paris 6, 2010. http://www.theses.fr/2010PA066733.
Der volle Inhalt der QuelleZarubica, Ana. „Influence du transporteur ABCA1 sur le microenvironnement lipidique de la membrane plasmique“. Aix-Marseille 2, 2009. http://theses.univ-amu.fr.lama.univ-amu.fr/2009AIX22025.pdf.
Der volle Inhalt der QuelleThe ABCA1 transporter is involved in the Apo A-I/mediated removal of cellular phospholipids and cholesterol at the cell membrane. Considering that ABCA1 acts as lipid translocator we investigated the effect of the transporter on membrane lipid microenvironment. By biochemical assays, we demonstrated that the ATP-ase activity of ABCA1 modifies the partitioning in lipid rafts of the transporter itself and other membrane proteins such as the transferrin receptor (TfR), TfR dynamic kinetics and down regulates TfR-mediated endocytosis. We then assessed by biophysical methods, cationic sensors and FLIM, significant modifications of membrane attributes at the inner and outer leaflet in the presence of ABCA1. Furthermore, we evidenced overall changes in membrane dynamics in the presence of ABCA1 by FRAP. Finally, we correlate the mechanistic basis of ABCA1-dependent modulation of macrophage phenotype with the influence of ABCA1 on lipid raft dependent signaling downstream of IFNγR
Mathey, Aline. „Nouvelles stratégies thérapeutiques et chimiorésistance : molécules bioactives et métabolisme lipidique“. Electronic Thesis or Diss., Bourgogne Franche-Comté, 2023. http://www.theses.fr/2023UBFCI014.
Der volle Inhalt der QuelleMany therapeutic failures persist due to adaptation and tumor resistance mechanisms, such as insensitivity to cell death signals, the overexpression of drug efflux transporters (i.e. ABC transporters involved in the multidrug resistance phenotype or MDR), mutations in DNA damage detection and repair pathways or reprogramming of energy metabolism. More specifically, an increasing number of studies suggest that deregulations of mitochondrial lipid metabolism, cardiolipins, play a role in tumor progression and aggressiveness, thereby representing an attractive therapeutic target in recent years. As a result, new innovative therapeutic protocols based on the use of bioactive molecules of low toxicity have appeared in order to overcome chemoresistance, reduce toxicity, side effects and potentiate the effectiveness of the chemotherapeutic drug in order to extend the life expectancy and enhance the quality of life of patients. Concerning the first part of this project, we demonstrated for the first time the ability of xanthohumol, a prenylated flavonoid extracted from hops, to restore the induction of DNA damage in colorectal cancer cells and to sensitize the latter to a commonly used clinically anticancer agent, SN38. We have also shown the ability of two essential oils extracted from Apiaceae in Tunisia, Pituranthos chloranthus and Teucrium ramosissimum, to restore the sensitivity of uterine sarcoma cells presenting the MDR phenotype, in particular to doxorubicin, mediated by the induction of apoptosis, the decrease in the overexpression and activity of the ABC transporter P-gp. The work resulting from the second part of this project provided a deeper insight into the existing relationships between cardiolipin metabolism and chemoresistance thanks to the identification of alterations in content, composition of cardiolipins and key molecular factors which represent new potential therapeutic targets in order to restore the sensitivity of tumors to chemotherapies
Auriac, Anne. „Les « rafts », radeaux lipidiques membranaires, participent à la régulation du transporteur de fer, la ferroportine, dans les macrophages“. Paris 11, 2010. http://www.theses.fr/2010PA112085.
Der volle Inhalt der QuelleIron is an essential element for the organism but can become toxic when present in excess. A proper regulation of iron absorption (in the duodenum) and iron recycling (in tissues macrophages) is therefore necessary. Hepcidin, a small peptide produced by hepatocytes, is involved in this systemic regulation. In fact, hepcidin induces the endocytoses and the degradation of ferroportin, the only known iron exporter in mammals. In this thesis, we studied the subcellular localization and the regulation of macrophage ferroportin and we looked forward potentials functional or regulatory partners of this exporter. We showed that ferroportin is localized in lipid rafts at the cell surface of macrophages. Furthermore, disruption of lipid rafts causes a decrease in the hepcidine induced ferroportin degradation. Cellular iron export seems to involve a ferroxidase named ceruloplasmin. We observed that cultured mouse macrophages produce a cytosolic and a GPI (glycosylphosphatidylinositol) anchored membrane ceruloplasmin. The expression of both forms of ceruloplasmin and ferroportin is strongly stimulated after iron treatment. Moreover, after iron treatment, the GPI-ceruloplasmin and ferroportin are co-expressed into lipid rafts. All together, our observations emphasize the role of lipid rafts in macrophage iron recycling. Finally, a proteomic approach of the ferroportin containing lipid rafts fractions pointed out some proteins which could be involved in the regulation and/or the activity of the macrophage ferroportin
Lhermusier, Thibault. „Régulation plaquettaire : ciblage de la protéine kinase Syk dans les HIT et rôle du transporteur lipidique ABCA1 dans les fonctions plaquettaires“. Toulouse 3, 2012. http://thesesups.ups-tlse.fr/1698/.
Der volle Inhalt der QuellePlatelet activation at sites of vascular injury is essential for haemostasis. Next to this critical role in bleeding arrest, platelets are involved in thrombotic diseases such atherothrombosis or heparin-induced thrombocytopenia (HIT). Therefore, they are targets of antithrombotic therapies. We have studied the mechanisms of platelet activation in two pathological situations; HIT with the tyrosine kinase Syk as a key player and Tangier disease resulting of a loss of function of the ABCA1 lipid transporter. HIT is a prothrombotic and potentially devastating complication of heparin therapy due to formation of platelet-activating antibodies directed against complexes of platelet factor 4 (PF4) and heparin. These antibodies contribute to clear platelet from the circulation and activate, by their Fc fragment, Fc?RIIA receptors on platelet surface or FcgRI and FcgRII receptors on monocyte, leading to platelet aggregation and tissue factor expression by monocytes. We have shown that Syk activation is crucial for platelet activation (signalization, secretion, aggregation, microparticle generation) initiated by anti-PF4/heparin antibodies from sera of patients suffering from HIT. Interestingly, Syk inhibition also prevented tissue factor expression and procoagulant activity of moncytic cells induced by these antibodies. We propose that Syk inhibitors, initially developed as a potential treatment of autoimmune disease, may be of therapeutic interest in the treatment of HIT. ABCA1 has been demonstrated to be crucial in the reverse cholesterol transport pathway by loading cholesterol and phospholipids into ApoA-I to generate high density lipoproteins. Its defect is associated to circulating lipid disturbance but also to hemorrhagic diathesis. Surprisingly, using ABCA1 knock-out mice, we have demonstrated that this transporter is neither implicated in phosphatidyserine exposure, a mechanism leading to the procoagulant activity of activated platelets, nor in the control of platelet membranes cholesterol content. However, mouse platelets deficient for ABCA1 have an increased size and a defect in response to low doses of agonists such as thrombin and collagen. Our data indicate that ABCA1 is involved in the efficiency of platelet signal transduction, particularly in the activation of Akt. These studies have characterized key players of platelet activation and suggest new strategies in the development of antithrombotic therapies
Lopez-Montero, Ivan. „Translocation de lipides non marqués mesurée par changements de forme de vésicules géantes : le cas de la céramide“. Paris 7, 2006. http://www.theses.fr/2006PA077189.
Der volle Inhalt der QuelleA 0. 1% of surface asymmetry between both monolayers of giant vesicles (GUVs) suffices to trigger shape changes in vesicles. The incorporation of exogenous molecules to the external leaflet of vesicles produces a shape change from prolate to pear that is reversed when the molecules redistribute in both monolayers, by transmembrane diffusion (flip-flop). The spontaneous flip-flop half-time of unlabelled molecules can be inferred by measuring the time of both shape transitions. A half-time for unlabeled ceramide (C6-Cer, C10-Cer, C16-Cer) flip-flop below 1 min at 37°C was measured. The method was validated by spectroscopic measures (EPR) of labelled ceramide flip-flop in LUVs. Shape changes in vesicles can also be used to detect the flip-flop of endogenous lipid by the action of a flippase protein. A purified P-gP and the Aminophospholipid Translocase were reconstituted into GUVs. The protein activation by the addition of external ATP produced vesicle shape changes according to an active lipid transport
Layeghkhavidaki, Hamed. „Effet des polluants de type hydrocarbures aromatiques polycycliques sur l'homéostasie lipidique et les récepteurs des lipoprotéines hépatiques“. Thesis, Université de Lorraine, 2014. http://www.theses.fr/2014LORR0120/document.
Der volle Inhalt der QuelleObesity is a multifactorial disorder that represents a significant risk factor for many pathologies including cardiovascular diseases, diabetes and neurodegenerative diseases. Recent epidemiological studies suggest potential obesogenic effects of environmental contaminants, but little information is available on their potential effect on hepatic lipoprotein metabolism. The objective of this study was to determine the effect of the common environmental pollutants, belonging to polycyclic aromatic hydrocarbon (HAP) on three lipoprotein receptors, the LDL-receptor (LDL-R), the scavenger receptor B1 (SRB1) and the lipolysis-stimulated lipoprotein receptor (LSR) as well as the ATP binding cassette transporters A1 (ABCA1) and G1 (ABCG1) using cell and/or animal models. Immunoblot and immunofluorescence in vitro studies revealed that exposure of Hepa1-6 to benzo[a]pyrene (B[a]P) significantly decreased LSR, LDL-R and ABCA1 protein levels, whereas no significant changes in protein levels and LSR activity where observed upon cell treatment with pyrene or phenanthrene. Real-time PCR analysis, lactacystin and chloroquine studies revealed that this effect was due primarily to increased proteasome-mediated degradation rather than to decreased transcription or to increased lysosomal degradation. Furthermore, ligand blots revealed that lipoproteins exposed to B[a]P displayed markedly decreased binding to LSR or LDL-R. C57Bl/6RJ mice were treated with B[a]P (0.5 mg/kg, i.p) every 48 h for 15 days. The increased weight gain observed was accompanied by increased plasma triglycerides and cholesterol levels, increased liver cholesterol content, and decreased LDL-R, ABCA1, ABCG1 and SR-B1 protein levels in B[a]P-treated animals as compared to controls. Correlations observed between hepatic LSR and LDL-R levels in control mice were no longer observed in B[a]P treated mice, suggesting a potential dysregulation of hepatic lipoprotein metabolism.Taken together, these results suggest that B[a]P-induced weight gain may be due its inhibitory action on LSR and LDL-R, as well as ABCA1 and lipoprotein metabolism in the liver, which leads to the modified lipid status in B[a]P-treated mice, thus providing new insight into mechanisms underlying the involvement of pollutants such as B[a]P in the disruption of lipid homeostasis, potentially contributing to dyslipidemia associated with obesity