Literatura académica sobre el tema "Dégradation lysosomale"
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Artículos de revistas sobre el tema "Dégradation lysosomale":
Galais, Mathilde, Baptiste Pradel, Isabelle Vergne, Véronique Robert-Hebmann, Lucile Espert y Martine Biard-Piechaczyk. "La phagocytose associée à LC3 (LAP)". médecine/sciences 35, n.º 8-9 (agosto de 2019): 635–42. http://dx.doi.org/10.1051/medsci/2019129.
Benbellal, Amina, Hanène Belabbassi, Sarrah Ait Ziane y Houria Kaced. "Management of type IV A mucopolysaccharidosis or Marquio A syndrome (A case report)". Batna Journal of Medical Sciences (BJMS) 6, n.º 2 (30 de diciembre de 2019): 121–24. http://dx.doi.org/10.48087/bjmscr.2019.6209.
Marcaillou, C., M. Truchet y R. Martoja. "Rôle des cellules S de l'épithélium caecal des Crustacés Isopodes dans la capture et la dégradation de protéines hémolymphatiques, et dans le stockage de catabolites (acide urique, sulfure de cuivre, phosphates)". Canadian Journal of Zoology 64, n.º 12 (1 de diciembre de 1986): 2757–69. http://dx.doi.org/10.1139/z86-400.
Tesis sobre el tema "Dégradation lysosomale":
Balfourier, Alice. "Biotransformations, dégradation et cycle de vie des nanoparticules d'or en milieu intracellulaire". Thesis, Université de Paris (2019-....), 2019. https://theses.md.univ-paris-diderot.fr/BALFOURIER_Alice_va2.pdf.
Gold nanoparticles display unique optical properties, and are considered as promising devices for medical imaging, therapy and diagnostic. Nevertheless, nanoparticles life cycle is still poorly understood at the cellular range. On the short term, nanoparticles are internalized by cells and sequestrated into the lysosomes, which are the intracellular vesicles responsible for the degradation and recycling of damaged endogenous and exogenous compounds. We focus our study on this step of nanoparticle life cycle, and more precisely on the lysosome and its nanoparticles content. Firstly, we studied this system from the lysosome point of view, and the impact of gold nanoparticles on its structural and functional integrity. Secondly, we considered the nanoparticles point of view, and the biotransformation they undergo in the lysosome. Once sequestrated into the lysosome, nanoparticles aggregate which modulate their optical properties, and thus modify their therapeutic potential. In order to capture this first biotransformation, we characterized the nature of these intracellular aggregates, and highlight the therapeutic potential of gold nanosphere aggregates, while they are considered as medically irrelevant when dispersed. Finally, we focus our study on the fate of gold nanoparticles in cells during six months. We demonstrate that gold nanoparticles were degraded in vitro, despite the current dogma that assert that gold nanoparticles are bio-inert. This process was proven to take place within days, and to be followed by the recrystallization of released gold. Transcriptomics analysis of the biological pathways activated in this biodegradation reveals the biological actors involved in this transformation, and to identify similarities between the response to gold nanoparticles and ionic gold, suggesting a common gold metabolism. This analogy opens up new prospects for the understanding of gold nanoparticle life cycle, but also for therapy. To conclude, the work presented in this thesis put into light new steps in gold nanoparticles life cycle, that enable us to propose therapeutic strategy that take advantages from fortuitous phenomena, while keeping in mind nanotoxicological issues
Delage, Laure. "Des déficiences génétiques comme modèles naturels pour l'étude de la régulation des checkpoints immunitaires et la caractérisation des réponses auto-immunes". Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5190.
Recessive NBEAL2 mutations have been reported in patients with Gray Platelet Syndrome (GPS). This syndrome is characterized by a macro-thrombocytopenia, with platelets lacking alpha-granules, leading to bleeding disorders, often associated with splenomegaly. Thus, NBEAL2 plays a crucial role in the trafficking of alpha-granules in platelets. Moreover, our lab has also described NBEAL2 deficiencies in patients presenting clinical features of the autoimmune lymphoproliferative syndrome, suggesting a role of NBEAL2 in immune homeostasis and tolerance. A broader international cohort of GPS patients has been described, revealing immune system abnormalities (autoimmune diseases, autoantibodies, lymphopenia). If the role of NBEAL2 in the traffic of granules is often investigated, the exact mechanism leading to the development of autoimmune manifestations in GPS patients remains unknown. NBEAL2 belongs to a protein family involved in vesicular trafficking, all of which possess a conserved BEACH domain. Within this BEACH-domain containing proteins family, one of the closest members to NBEAL2 is LRBA. LRBA is involved in the recycling of CTLA-4, an inhibitory immune checkpoint. CTLA-4 plays a crucial role in the regulation of immune responses and tolerance. Recessive mutations of LRBA lead to similar clinical features as partial CTLA-4 deficiency: autoimmunity, lymphocytic infiltrations, and progressive B lymphopenia. Physiologically, LRBA prevents the lysosomal degradation of CTLA-4 and allows its recycling to the membrane. By analogy with LRBA, we investigated the importance of NBEAL2 in immune checkpoints intracellular trafficking and we brought new insights on its role in lymphocytes. Thus, NBEAL2 is a scaffold protein, binding LRBA, and involved in CTLA-4 trafficking as well as in vesicular trafficking in general. This work brings new knowledge to the regulation of CTLA-4 in activated T lymphocytes, a list of new partners for NBEAL2 protein and a new model of vesicular trafficking in which NBEAL2 is involved. Finally, a better understanding of the mechanisms leading to autoimmunity in patients with gray platelets syndrome could lead to better diagnosis and treatment management
Bifsha, Panojot. "Implication de la voie de dégradation ubiquitine-dépendante dans la pathologie des maladies de surchage lysosomale". Thèse, 2005. http://hdl.handle.net/1866/15199.