Academic literature on the topic 'Récepteurs glucocorticoïdes'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Récepteurs glucocorticoïdes.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Récepteurs glucocorticoïdes":
Riguen, M., H. Chaker, N. Dammak, S. Toumi, A. Kammoun, H. Makni, T. Boudawara, S. Yaich, K. Kammoun, and M. Ben Hmida. "Apport de l’expression rénale des récepteurs aux glucocorticoïdes en immunohistochimie au cours du syndrome néphrotique idiopathique." Néphrologie & Thérapeutique 17, no. 5 (September 2021): 330. http://dx.doi.org/10.1016/j.nephro.2021.07.212.
Ben Rhouma, K., S. Schimchowitsch, M. E. Stoeckel, J. M. Felix, and M. Sakly. "Implication des Récepteurs Glucocorticoïdes de Type II dans l'Action Apoptotique de l'Aldostérone sur les Thymocytes de Rat." Archives of Physiology and Biochemistry 105, no. 2 (January 1997): 216–24. http://dx.doi.org/10.1076/apab.105.2.216.12919.
Laulhé, M., E. Pussard, J. Perrot, P. Kamenicky, M. Lombes, S. Viengchareun, and L. Martinerie. "Polymorphisme du gène du récepteur glucocorticoïde (nr3c1) et hypersensibilité aux glucocorticoïdes : mécanismes moléculaires de l’insuffisance corticotrope glucocorticoïde-induite." Annales d'Endocrinologie 82, no. 5 (October 2021): 261. http://dx.doi.org/10.1016/j.ando.2021.08.026.
Prin, L., P. Lefebvre, V. Gruart, M. Capron, L. Storme, P. Formstecher, S. Loiseau, and A. Capron. "Polynucléaire éosinophile et récepteur glucocorticoïde." Revue Française d'Allergologie et d'Immunologie Clinique 30, no. 2 (April 1990): 83–85. http://dx.doi.org/10.1016/s0335-7457(05)80216-3.
Boullu, S., JG Velut, C. Oliver, and M. Grino. "L'isoforme β du récepteur des glucocorticoïdes : un facteur de résistance aux glucocorticoïdes ?" médecine/sciences 14, no. 6-7 (1998): 812. http://dx.doi.org/10.4267/10608/1147.
Roumestan, C., C. Gougat, D. Jaffuel, and M. Mathieu. "Les glucocorticoïdes et leur récepteur : mécanismes d'action et conséquences cliniques." La Revue de Médecine Interne 25, no. 9 (September 2004): 636–47. http://dx.doi.org/10.1016/j.revmed.2004.01.012.
Vilarem, MJ. "Un antituberculeux, la rifampicine : ligand et activateur du récepteur des glucocorticoïdes." médecine/sciences 14, no. 4 (1998): 451. http://dx.doi.org/10.4267/10608/1061.
Kahn, A., and JC Dreyfus. "Le récepteur des glucocorticoïdes... et son homologie avec l'oncogène v-erb-A." médecine/sciences 2, no. 3 (1986): 151. http://dx.doi.org/10.4267/10608/3461.
Vitellius, G., J. Bouligand, J. Fagart, F. Castinetti, A. Guiochon Mantel, B. Delemer, S. Trabado, and M. Lombès. "Trois mutations originales du récepteur des glucocorticoïdes révélées par un incidentalome surrénalien." Annales d'Endocrinologie 76, no. 4 (September 2015): 320. http://dx.doi.org/10.1016/j.ando.2015.07.090.
Dalle, H., M. Garcia, T. Ledent, T. T. H. Do, M. Buyse, R. Denis, S. Luquet, B. Fève, and M. Moldes. "Rôle du récepteur des glucocorticoïdes adipocytaire dans la lipodystrophie induite par la corticostérone." Annales d'Endocrinologie 77, no. 4 (September 2016): 294. http://dx.doi.org/10.1016/j.ando.2016.07.907.
Dissertations / Theses on the topic "Récepteurs glucocorticoïdes":
Sablonnière, Bernard. "Organisation hétéro-oligomérique du récepteur des glucocorticoi͏̈des." Lille 1, 1988. http://www.theses.fr/1988LIL10117.
Ambroggi, Frédéric. "Identification de la cible cellulaire des effets des glucocorticoïdes." Bordeaux 2, 2005. http://www.theses.fr/2005BOR21303.
Lustenberger, Patrick. "La chromatographie d'affinité des récepteurs des hormones stéroïdes : application à la purification du récepteur des glucocorticoi͏̈des du foie de lapin." Lille 1, 1986. http://www.theses.fr/1986LIL10137.
Belahsen, Youness. "Purification et caractérisation du récepteur des glucocorticoïdes sous forme transformée." Lille 1, 1987. http://www.theses.fr/1987LIL10045.
Carillo, Conesa María-Ángeles. "Le rôle des glucorticoïdes et du récepteur des glucorticoïdes dans les processus de neurodegenerescence et d'inflammation dans le Système Nerveux Central." Paris 6, 2011. http://www.theses.fr/2011PA066688.
Kootar, Scherazad. "L’importance des récepteurs aux glucocorticoïdes dans la physiopathologie de la maladie d’Alzheimer." Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4015/document.
Strong evidence shows that oligomeric forms of the amyloid-ß peptide (oAß) cause synapse dysfunction promoting loss of hippocampus-dependent memories in the early phase of Alzheimer’s disease (AD). AD is also associated with Hypothalamus-Pituitary-Adrenal (HPA) axis dysfunction which results in an increase of glucocorticoids (CORT) activating glucocorticoid receptors (GRs). We showed that subchronic GR antagonist in 4 month Tg2576 (Tg+) mice could rescue the synaptic deficit and memory impairment (Lanté et al., 2015).In this context, we studied the contribution of GRs to AD physiopathology. Dysregulated HPA axis was characterized by increased CORT levels at 4 and 6 months of age and by loss of CORT feedback inhibition in the Tg+ mice. We further crossed the Tg+ with GRlox/lox to produce GRlox/loxTg+ mice. These mice innately exhibited high CORT levels from weaning period and due to other several unforeseen reasons, we discontinued using this new mouse model. Instead, to identify the functional relationship between the GRs and oAß at synapses, we shifted to acute oAß treatment in neurons in vitro and ex-vivo hippocampus slices. In neuron cultures, GR levels increased in the post synaptic density upon acute oAß treatment. Further, treatment of oAß on ex-vivo hippocampus slices after either pharmacological blocking of GR or genetic ablation, prevented the oAβ-dependent LTP impairment. To conclude, our results with the Tg+ mice suggest that a neuroendocrine dysregulation occurs during the onset of AD pathology. Additionally, we have evidence for a functional relationship between oAß and GRs with GRs at the synapse playing an important role in acute Aß-induced synapto-toxicity
Kootar, Scherazad. "L’importance des récepteurs aux glucocorticoïdes dans la physiopathologie de la maladie d’Alzheimer." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4015.
Strong evidence shows that oligomeric forms of the amyloid-ß peptide (oAß) cause synapse dysfunction promoting loss of hippocampus-dependent memories in the early phase of Alzheimer’s disease (AD). AD is also associated with Hypothalamus-Pituitary-Adrenal (HPA) axis dysfunction which results in an increase of glucocorticoids (CORT) activating glucocorticoid receptors (GRs). We showed that subchronic GR antagonist in 4 month Tg2576 (Tg+) mice could rescue the synaptic deficit and memory impairment (Lanté et al., 2015).In this context, we studied the contribution of GRs to AD physiopathology. Dysregulated HPA axis was characterized by increased CORT levels at 4 and 6 months of age and by loss of CORT feedback inhibition in the Tg+ mice. We further crossed the Tg+ with GRlox/lox to produce GRlox/loxTg+ mice. These mice innately exhibited high CORT levels from weaning period and due to other several unforeseen reasons, we discontinued using this new mouse model. Instead, to identify the functional relationship between the GRs and oAß at synapses, we shifted to acute oAß treatment in neurons in vitro and ex-vivo hippocampus slices. In neuron cultures, GR levels increased in the post synaptic density upon acute oAß treatment. Further, treatment of oAß on ex-vivo hippocampus slices after either pharmacological blocking of GR or genetic ablation, prevented the oAβ-dependent LTP impairment. To conclude, our results with the Tg+ mice suggest that a neuroendocrine dysregulation occurs during the onset of AD pathology. Additionally, we have evidence for a functional relationship between oAß and GRs with GRs at the synapse playing an important role in acute Aß-induced synapto-toxicity
Burollaud, Thierry. "Etude du site actif du récepteur des glucocorticoi͏̈des : modalités comparées de son interaction avec les stéroi͏̈des agonistes et antagonistes." Lille 1, 1993. http://www.theses.fr/1993LIL10091.
Formstecher, Pierre. "Le site de liaison aux stéroi͏̈des du récepteur des glucocorticoïdes : caractérisation à l'aide de sondes moléculaires diverses." Lille 1, 1986. http://www.theses.fr/1986LIL10136.
Muller, Caroline. "Etude du mécanisme d'action anti-glucocorticoïde des dérivés 7-hydroxylés de la déhydroépiandrostérone." Paris, CNAM, 2006. http://www.theses.fr/2006CNAM0554.
Experiments with a confocal microscope with a COS cell line transfected with the human glucocorticoid receptor (hGR) showed that dehydroepiandrosterone (DHEA) and its 7-hydroxylated derivatives do not modify the location of the receptor and do not prevent the nuclear transfer of hGR. These steroids had no effect on the transactivation activity of hGR. Thus, these neurosteroids were inactive on this model and their genomic action through the GR could be excluded. The human 11β-hydroxysteroid dehydrogenase type 1 (h11β-HSD1) was expressed in the yeast and each of the enzyme-catalyzed reactions were analyzed. The inter-conversion of the 7-hydroxylated DHEA metabolites was demonstrated as well as the oxidoreduction of cortisol and cortisone. A competition for the binding with the h11β-HSD1 may take place between these steroids and the glucocorticoid activation process, the former triggering immunity and the latter suppressing it