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Статті в журналах з теми "Récepteur de la Kisspeptine-1":
Begon, Emmanuelle, and Valérie Bernard. "La prolactine et son récepteur : Des modèles animaux à la physiopathologie hypophysaire." Biologie Aujourd’hui 216, no. 3-4 (2022): 105–10. http://dx.doi.org/10.1051/jbio/2022019.
Bellina, Mélanie, and Agnès Bernet. "La nétrine-1, une nouvelle cible antitumorale." médecine/sciences 38, no. 4 (April 2022): 351–58. http://dx.doi.org/10.1051/medsci/2022038.
De Meyts, Pierre. "Le récepteur de l’insuline a 50 ans – Revue des progrès accomplis." Biologie Aujourd’hui 216, no. 1-2 (2022): 7–28. http://dx.doi.org/10.1051/jbio/2022007.
Dieu-Nosjean, Marie-Caroline, and Christophe Caux. "La biologie des cibles PD-1 et CTLA-4 et la question des biomarqueurs." médecine/sciences 35, no. 12 (December 2019): 957–65. http://dx.doi.org/10.1051/medsci/2019192.
Gorry, P. R., and C. Zhang. "HIV 1: le récepteur CCR5, voie vaccinale potentielle." Revue Française des Laboratoires 2003, no. 349 (January 2003): 14. http://dx.doi.org/10.1016/s0338-9898(03)80448-1.
Poisbeau, P. "Pharmacologie des anxiolytiques." European Psychiatry 30, S2 (November 2015): S8. http://dx.doi.org/10.1016/j.eurpsy.2015.09.032.
Mehlen, P., V. Corset, and A. Chédotal. "Le récepteur de l'adénosine A2b : un co-récepteur de la nétrine-1 impliqué dans le guidage axonal." médecine/sciences 17, no. 2 (2001): 238. http://dx.doi.org/10.4267/10608/1901.
Hamon, M. "Bases neurobiologiques des traitements de l’alcoolo-dépendance – Quelles perspectives ?" European Psychiatry 29, S3 (November 2014): 539. http://dx.doi.org/10.1016/j.eurpsy.2014.09.411.
Chabbert-Buffet, N. "Modulateurs du récepteur de la progestérone." EMC - Gynécologie 4, no. 3 (January 2009): 1–11. http://dx.doi.org/10.1016/s0246-1064(09)44671-1.
Alizon, M. "Entrée de VIH-1 : un récepteur orphelin est adopté." médecine/sciences 12, no. 10 (1996): 1185. http://dx.doi.org/10.4267/10608/649.
Дисертації з теми "Récepteur de la Kisspeptine-1":
Delli, Virginia. "Exploring the contribution of NO-synthesizing neurons in the set-in motion and the functioning of the hypothalamus-pituitary-gonadal axis." Electronic Thesis or Diss., Université de Lille (2022-....), 2023. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2023/2023ULILS085.pdf.
The nitric oxide (NO) signaling pathway in hypothalamic neurons plays a pivotal role in regulating the release of gonadotropin-releasing hormone (GnRH). GnRH, the primary regulator of the hypothalamic-pituitary-gonadal (HPG) axis, holds authority over fertility and reproduction. The maturation of the HPG axis is a crucial phase in establishing reproductive function.Our research has contributed in the characterization of the first postnatal activation of the HPG axis, or minipuberty. We identified sex differences in the timing of minipuberty in mice, with neuronal nitric oxide synthase (nNOS) activity in the preoptic region playing a pivotal role in this process. Estrogen significantly contributes to the activation of preoptic nNOS, although it appears to involve gonadal sources in females, but not in males. The sex-specific timing of NOS1 activity proves essential for the proper activation of the HPG axis during minipuberty, and its absence leads to GnRH deficiency and lifelong sensory and intellectual comorbidities in both humans and mice. Intriguingly, NO replenishment therapy during minipuberty successfully rescues both reproductive and non-reproductive comorbidities in Nos1-deficient mice.In adulthood, GnRH exhibits two distinct secretion profiles that oscillate over days, orchestrating the estrous cycle in the form of pulses and surges. The mechanisms governing these tonic and phasic modes remain a topic of ongoing debate.Our studies revisited and challenged the prevailing notion of kisspeptin as an absolute "monarch”, proposing the concept of a Kisspeptin-nNOS-GnRH, or "KiNG," network responsible for generating the "GnRH pulse" and "GnRH surge." We demonstrate that the nNOS population in the OV/MePO is indispensable for the kisspeptin-induced GnRH activation and subsequent luteinizing hormone (LH) secretion, primarily through the Kisspeptin receptor/phospho-nNOS/cGMP pathway. Thus, we provide insights into the KiNG network, strongly suggesting that NO/Kisspeptin interaction is a critical component for precise regulation of GnRH/LH release. NO signaling in the preoptic area fine-tunes Kisspeptin's impact on GnRH neurons
Renaudo, Adrien. "Récepteur Sigma-1, canaux logiques et régulation du cycle cellulaire." Nice, 2006. http://www.theses.fr/2006NICE4024.
During the 20th century, cancer has emerged as a major public health problem. Nowadays, it's the second cause of mortality in France. Faced with such a stake, many research pathways are curently explored. In the last decade, a growing number of studies have put in the light the implication of ionic channels in cellular migration, proliferation and death. If the precise function of ionic channels in these phenomenon is still unclear, there's no doubt about their interest within the framework of cancer. Some of these studies underline more specifically the implication of the K+ and Cl- channels which are presiding to cell volume regulation (RVD). An other protein, the sigma-1 receptor, is begining to draw the attention of researchers. It's a protein of 26 kDa, mostly localised at the RE and MP membranes and only related to a yeast C8-C7 sterol isomerase. Interestingly, the sigma-1 receptor is overexpressed in tumour cells. However, the reason of this overexpression remains enigmatic. Recently, Soriani has shown that sigma-1 receptor inhibit K+ channels (Soriani et al, 1998). That's why we decided to explore a putative link between sigma-1 receptor, ionic channels (K+ et Cl-) and tumour cell proliferation. In this work, we used pulmonary tumour cells (SCLC) and acute T-leucemic cells (Jurkat). For the first time, we have demonstrated that pharmacological activation of the sigma-1 receptor with specific ligands arrests cell proliferation in the G1 phase of the cell-cycle. This inhibition of proliferation is underlined by an increase in p27kip1 (a cell cycle inhibitor) and a decrease in cyclin A (a S phase key protein) expression levels. Our results indicate that this arrest is based on the inhibition of two famillies of ionic channels crucials for cell volume regulation : voltage-dependant K+ channels (Kv) and Cl- channels of the ICl,swell family. It's the first time that an inhibition of Cl- channels by sigma-1 receptors is demonstrated. In other respects, sigma-1 receptor overexpression in HEK cells alters the kinetic properties of ICl,swell leading to a slow down of volume regulation process. Therefore, when cells are submitted to an apoptotic stress, the AVD (Apoptotic Volume Decrease) is partially inhibited and cells are protected against apoptosis. Those results might explain the overexpression of the sigma-1 receptor in tumour's cells
Auger-Messier, Mannix. "Mécanisme moléculaire d'activation du récepteur AT[indice]1 de l'angiotensine II." Mémoire, Université de Sherbrooke, 2001. http://savoirs.usherbrooke.ca/handle/11143/3244.
Lamouille, Samy. "Effets biologiques et mécanismes d'action du récepteur ALK-1 dans l'angiogenèse." Université Joseph Fourier (Grenoble), 2004. http://www.theses.fr/2004GRE10008.
Bencheikh, Laura. "Fonctions nucléaires du récepteur de CSF-1 dans les monocytes humains." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS426/document.
CSF-1R (colony-stimulating factor 1 receptor) is a transmembrane receptor with a tyrosine kinase activity. It is expressed at the cell surface of monocytes, macrophages and their progenitors. Its ligand, CSF-1, has an instructive role on hematopoietic stem cells to direct their differentiation into the myeloid lineage. CSF-1R is also able to differentiate monocytes into macrophages. A nuclear location was described for CSF-1R in cancer cell lines, primary breast tumors and murine macrophages. In the cell nucleus, CSF-1R was suggested to regulate nuclear protein phosphorylation and gene expression. We demonstrate that a small part of CSF-1R is in the nucleus of primary human monocytes, using different antibodies and technical approaches. Nuclear CSF-1R corresponds to full length monomeric receptor. After activation by its ligand, CSF-1R is translocated form cell surface to the nucleus through a retrograde transport, together with CSF-1. Kinase activity inhibitors impaired this process while inhibitors of CRM1-dependant nuclear export (leptomycin B) can revert this effect. In monocytes, CSF-1R is localized on chromatin, mainly on intergenic and intronic regions. It colocalizes with H3K4me1 mark which signs active enhancers. The receptor is present around genes involved in morphogenesis, nervous system development, ossification and cell differentiation. CSF-1R is also located on PU.1 promoter, which is a master transcription factor involved in myeloid and monocyte differentiation. CSF- 1R is also present on genes implicated in macrophage functions, differentiation, polarization and survival. At the chromatin level, CSF-1R interacts with different transcription factors like EGR1 and exerts a co-repressive role to decrease or limit gene expression. CSF-1R nuclear localization persists in macrophages generated by exposure of monocytes to CSF-1. It entails CSF-1R relocalization on promoter-TSS and exonic regions where it colocalizes with H3K4me3 mark. The receptor is close to genes regulating vascularization, phagocytosis, metabolism, stress and hypoxia responses. CSF-1R interacts with ELK1 and YY1 to promote macrophage functions. When monocytes are differentiated into macrophages with GM-CSF, CSF-1R also remains in the nucleus. However, its chromatin localization and interactions change compared to monocytes and CSF-1 differentiated macrophages. This indicates that nuclear CSF-1R is differentially regulated, depending on the cytokine that triggers cell differentiation. In monocytes from chronic myelomonocytic leukemia, CSF-1R expression, chromatin localization and interactors are modified, indicating a deregulated CSF-1R nuclear function under pathological state. Altogether, we showed that CSF-1R is localized in the nucleus of human monocytes and macrophages where it regulates gene expression including PU.1. Preliminary results suggest CSF-1R nuclear location in myeloid progenitor subsets where the receptor could directly regulate the expression of myeloid differentiation genes. Targeting CSF-1R is currently tested as a therapeutic strategy to impair tumor infiltrating macrophages. Our results show that CSF-1R inhibitors are able to target both membrane and nuclear forms and thus to inhibit all CSF-1R activities in the cells, enhancing the potential therapeutic effects of these molecules
Chavagnieux, Cédric. "Développement d'un récepteur hybride GPS/GALILEO en environnement réel." Mémoire, École de technologie supérieure, 2007. http://espace.etsmtl.ca/564/1/CHAVAGNIEUX_C%C3%A9dric.pdf.
Larrivée, Jean-François. "Étude de la régulation des récepteurs B¦1 et B¦2 des kinines et caractérisation pharmacologique de nouveaux antagonistes du récepteur B¦1 chez le lapin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ60774.pdf.
St-Louis, Etienne. "Étude des mécanismes de rétention du récepteur opioïde delta." Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/9852.
Jaillard, Céline. "Edg8/s1p5 : récepteur bi-fonctionnel de l' oligodendrocyte." Paris 6, 2005. http://www.theses.fr/2005PA066595.
Moreno, Sébastien. "Le récepteur 3 de la neurotensine/Sortiline dans la régulation de l’état dépressif." Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4136/document.
Major depressive disorder is a condition that affects 20% of the population and is the leading cause of morbidity and disability worldwide. Recently, the TREK-1 potassium channel has been shown to be a potential target in the treatment of depression. The deletion of this channel or its blocking by a derived peptide resulting from the maturation of Sortilin, propeptide (PE), or its synthetic analogue Spadin, results in a phenotype of resistance to depression in mice. Sortilin is a protein able to bind with TREK-1 but also with the neurotrophic factor BDNF, an important factor for neuronal viability and depressive state regulation. Sortilin is therefore involved in regulating the intracellular addressing of TREK-1 and BDNF. Initially, my work focused on the consequences of the deletion of the Sortilin gene (sort1-/-) on the TREK-1 and BDNF addressing, and the neurotensinergic system. The results showed a decrease in TREK-1 membrane expression at the cerebral level and an increase in BDNF. All of these changes lead the Sort1-/- mice to develop a phenotype of resistance to depression. In addition, these mice show an increase in brain neurotensin concentration and its receptor 2, leading to increased resistance to pain perception. In a second phase, I was interested in whether PE, a potential antidepressant, showed serum variations in depressed patients and could be an indicator of depressive syndrome. We showed that the serum PE level is significantly reduced in depressed people, a level restored after treatment with antidepressants. In conclusion, Sortilin plays a major key in the regulation of depressive disorder and also in nociception
Частини книг з теми "Récepteur de la Kisspeptine-1":
Robert, Jacques. "Les récepteurs toll-like, l’interleukine 1 et le NFκB." In Signalisation cellulaire et cancer, 145–54. Paris: Springer Paris, 2010. http://dx.doi.org/10.1007/978-2-8178-0028-8_13.
"Développement d’un immunoconjugué cytotoxique ciblant le récepteur de l’IGF-1." In Chimie et nouvelles thérapies, 201–14. EDP Sciences, 2020. http://dx.doi.org/10.1051/978-2-7598-2478-6-013.
"Développement d’un immunoconjugué cytotoxique ciblant le récepteur de l’IGF-1." In Chimie et nouvelles thérapies, 201–14. EDP Sciences, 2020. http://dx.doi.org/10.1051/978-2-7598-2478-6.c013.
Robert, Jacques. "Récepteurs de l'interleukine 1 et récepteurs toll-like (TLR)." In Ciblage Thérapeutique en Oncologie, 73–74. Elsevier, 2023. http://dx.doi.org/10.1016/b978-2-294-77967-1.00011-5.
Bockaert, Joël. "Chapitre 1 : La chimie des récepteurs des neurotransmetteurs." In Chimie et cerveau, 17–32. EDP Sciences, 2020. http://dx.doi.org/10.1051/978-2-7598-1894-5-004.
Bockaert, Joël. "Chapitre 1 : La chimie des récepteurs des neurotransmetteurs." In Chimie et cerveau, 17–32. EDP Sciences, 2020. http://dx.doi.org/10.1051/978-2-7598-1894-5.c004.
Robert, Jacques. "Cytokines et récepteurs couplés à une activité tyrosine kinase." In Ciblage Thérapeutique en Oncologie, 43–47. Elsevier, 2023. http://dx.doi.org/10.1016/b978-2-294-77967-1.00006-1.