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Статті в журналах з теми "Mécanismes de détoxification cellulaire":
Leroux, J. C. "Mécanismes de détoxification attendus des technologies nouvelles." Toxicologie Analytique et Clinique 28, no. 3 (September 2016): 241–42. http://dx.doi.org/10.1016/j.toxac.2016.05.016.
Chartier, Nicolas T., Vincent Hyenne, and Jean-Claude Labbé. "Mécanismes de division cellulaire asymétrique." médecine/sciences 26, no. 3 (March 2010): 251–58. http://dx.doi.org/10.1051/medsci/2010263251.
Lacronique, J., F. Russo-Marie, and J. Marsac. "Mécanismes d'action cellulaire des glucocorticoïdes." Revue Française d'Allergologie et d'Immunologie Clinique 30, no. 4 (October 1990): 241–45. http://dx.doi.org/10.1016/s0335-7457(05)80263-1.
Peyriéras N. "Les mécanismes de l'adhérence moléculaire cellulaire." médecine/sciences 8, no. 7 (1992): 758. http://dx.doi.org/10.4267/10608/3223.
Vinzio, S., O. Morel, J. L. Schlienger, and B. Goichot. "Mécanismes d’action cellulaire des hormones thyroïdiennes." La Presse Médicale 34, no. 16 (September 2005): 1147–52. http://dx.doi.org/10.1016/s0755-4982(05)84141-7.
Widmann, Christian. "Mécanismes de survie au stress cellulaire." Revue Médicale Suisse 1, no. 17 (2005): 1141–46. http://dx.doi.org/10.53738/revmed.2005.1.17.1141.
Birsen, Rudy, Eric Grignano, Nicolas Chapuis, and Didier Bouscary. "Ferroptose et cancer." médecine/sciences 37, no. 8-9 (August 2021): 726–34. http://dx.doi.org/10.1051/medsci/2021108.
Moreaux, Jérôme. "Anticorps anti-CD38 dans le myélome multiple." médecine/sciences 35, no. 12 (December 2019): 1001–4. http://dx.doi.org/10.1051/medsci/2019198.
Gönczy, Pierre. "Mécanismes de division cellulaire : leçons d’un nématode." médecine/sciences 19, no. 6-7 (June 2003): 735–42. http://dx.doi.org/10.1051/medsci/20031967735.
Mercié, P., and F. Belloc. "Mécanismes physiopathologiques et méthodes d’analyse de l’apoptose cellulaire." La Revue de Médecine Interne 22, no. 1 (January 2001): 90–96. http://dx.doi.org/10.1016/s0248-8663(00)00297-6.
Дисертації з теми "Mécanismes de détoxification cellulaire":
Fleurbaix, Emmanuel. "Évaluation écotoxicologique des éléments terres-rares : approches cellulaires chez différentes espèces aquatiques." Electronic Thesis or Diss., Université de Lorraine, 2021. http://www.theses.fr/2021LORR0324.
Since 30 years ago, the growing use of Lanthanides in new technologies has contributed to important releases of these metals into aquatic ecosystems. In a global sustainable development policy aimed at preserving the quality of ecosystems, the impact of Lanthanides on aquatic organisms has naturally been questioned. However, studies on the aquatic ecotoxicology of Lanthanides are incomplete, and no consensus is established yet. In this context, we studied the cellular toxicity of Lanthanides individually and in mixtures. To determine these toxic effects, cell viability was measured on Danio rerio fibroblast-like cells (ZF4; ATCC®, CRL-2050™), Danio rerio hepatic cells (ZFL; ATCC®, CRL-2643™), Oncorhynchus mykiss epithelial cells (RTgill-W1; ATCC®, CRL-2523™), and primary culture of Corbicula fluminea digestive glands exposed to Lanthanides. Direct toxicity of Lanthanides has been observed on all cellular models. Concerning the toxicity of Lanthanides in mixtures, synergistic effects have been underlined on the three fish cell lines. In this research, we focused on the mechanisms of the detoxification of Lanthanides in the case of ZF4 cells from Danio rerio. The effects of Lanthanides were assessed in the presence of specific inhibitors of glutathione-S-transferases (ethacrynic acid) and MRP-like (MK571 and probenecid), by cell viability measurements. We decided to study these actors of the cellular detoxification due to their respective roles in phases II and III of the cellular detoxification of metals in fishes and bivalves. Regarding the results, MRP-like proteins are effectively involved in the detoxification of Lanthanides in ZF4 cells. Overall, our results highlighted the relevance of the toxic effects of Lanthanides at the cellular level for the risk assessment of these metals
Gava, Fabien. "Etude des mécanismes d'agrégation cellulaire tumorale." Thesis, Toulouse 3, 2018. http://www.theses.fr/2018TOU30372.
Metastases are responsible for 90% of cancer-related deaths justifying the current cancer research's substantial part dedicated to study their formation's mechanisms. It has been recently demonstrated that clusters (or aggregates) of circulating tumor cells (CTCs) identified in patient's blood samples have a far higher metastatic potential than isolated circulating tumor cells. It also has been shown that their detection is correlated with a poor prognosis for patients suffering from epithelial cancers. These observations open up promising diagnostic and therapeutic perspectives but that still requires further investigation on the mechanisms of clusters formation. In this context our laboratory developed an in vitro semi-automated assay based on video microscopy enabling the study of mechanisms involved in tumor cell anchorage-independent clustering. This assay allowed to demonstrate the involvement of adherent junction protein E-cadherin and desmosomal junction proteins DSG2 and DSC2 during tumor cell clustering. The aim of my work was to investigate epithelial intercellular junction's proteins involvement in tumor cell aggregation in anchorage-independent conditions and to search for new regulators. In the first instance I explored and demonstrated the role of communicating junctions (or gap junctions) and P-cadherin in tumor cell aggregation of breast and colorectal cancer cell lines. In the second part, I developed a strategy based on tumor cell lines classification depending on their characteristics of the aggregation process. With the aim of determining the parameters of this classification, I examined aggregation abilities of 28 tumor cell lines derived from epithelial cancers. This study provides evidence for a high variability during this process and allows defining cell lines categories integrating both aggregation process dynamic aspects and aggregates structure. The combination of this classification with current available expression data could lead to the identification of original new aggregation regulators. Together, these results have underscored new anchorage-independent tumor cell aggregation regulators and a wide range of behaviors of different tumor cell lines observed. Our work provides opportunities into a better understanding of involved mechanisms, towards an application to study circulating tumor cells from patients and also a therapeutic targeting of these clusters
Laporte, Fanny. "Compréhension des mécanismes de complexation de l'uranyle par les molécules du vivant : élaboration de peptides biomimétiques chélatants pour la détoxification." Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV038.
Heavy metals, especially actinides, are toxic for humans. Understanding the mechanisms responsible for their toxicity is an important field of research in toxicology. Uranyl toxicity is still not well understood. The understanding of uranyl interactions at the molecular level is necessary to predict its chemical toxicity and to develop efficient chelating agents. This work aims at identifying uranyl binding sites in proteins and key factors that govern these interactions. To obtain thermodynamic and structural data, strategies were developed to study two proteins predicted as major uranyl targets which present different structures and properties. We took advantage of fetuin-A structure and studied the two structured domain of the protein by complementary physico-chemical methods including multidimensional NMR spectroscopy to acquire structural information on uranyl binding sites in this protein. In order to elucidate interactions between the metal and disordered phosphorylated proteins such as osteopontin, we designed peptides preorganized in β-sheet optimized to coordinate uranyl cation. We introduced amino acids containing phosphate groups and demonstrated that these peptides are relevant models to mimic uranyl binding sites found in phosphorylated proteins. Biomolecules display different structures and properties which may constitute an obstacle to affinity studies. A tool based on a non-natural fluorescent probe was developed to investigate and compare uranyl targets affinities
Le, Bouffant Ronan. "Facteurs de traduction et mécanismes de surveillance du cycle cellulaire." Rennes 1, 2007. http://hal.upmc.fr/tel-01117521.
Cell division is a highly regulated process and when a problem occurs, the cell cycle checkpoints are activated. When cell cycle checkpoints are defective, pathological disease, as cancer, can occur. The implication of translation factors during checkpoints activation was studied in sea urchin embryo model. The work realized during this PhD demonstrated a functional DNA damage checkpoint during the first cell division of sea urchin embryo. The eIF2 phosphorylation was shown to be implicated in translational activation after fertilization and in translation inhibition after MMS treatment, a DNA alkylating molecule. This study shows an expression of functional 4E-BP protein, a translational inhibitor, after induction of DNA damages by radiomimetic drug (bleomycin), hypoxic stress or heavy metal (ChromeIII) treatment in sea urchin embryo. We demonstrated that, after MMS treatment, which doesn’t induced 4E-BP expression, the eIF4G protein was modified, degraded or cleaved as a function of drug dose. Our work support interest and knowledge on translational factors implication when checkpoint was mobilisated after DNA damages or cellular stress in sea urchin embryo. These results are a starting point to study new regulations of translational factors eIF4E, eIF4G and 4E-BP when cell is directed toward survival or cell death pathways
Escoffre, Jean-Michel. "Mécanismes moléculaires et cellulaire de l'électrotransfert de plasmides in vitro." Toulouse 3, 2010. http://thesesups.ups-tlse.fr/1296/.
Plasmid transfer within a target cell represents a key tool in the study of biological functions and the development of new therapeutic strategies. However, the transfer of plasmids must be carried out with a minimum of side effects on the level of the target cell. The technique of electropermeabilization is a physical method based on the modulation of the native transmembrane electric potential of the cell by an external electric field. However, the rational use of the electropermeabilization in pharmacology and medicine could be done only thanks to one perfect comprehension of the mechanisms involved in the electropermeabilization at the membrane level and its cellular consequences. The mechanism of the plasmid electrotransfer is a multi-steps process with a step of plasmid/membrane interaction during the application of the electric pulses, followed after these last, of a step of plasmid translocation through the plasma membrane. This multi-disciplinary research task aims at a better comprehension of the mechanism of the plasmid electrotransfer. It integrates the study of the membrane consequences of the electropermeabilization and the study of the plasmid/ membrane interaction. The application of milliseconds and permeabilizing electric pulses induces a membrane disorder and a fast phospholipid translocation in the permeabilized regions. The electro-induced translocation of phospholipids is not associated with a loss of cell viability. The existence of the multi-steps process of the plasmid electrotransfer (membrane permeabilization, plasmid/membrane interaction and gene expression) was confirmed in various cell lines. During the application of the first electric pulse, the plasmids migrate by electrophoresis and come to interact in distinct sites from the membrane region facing the cathode. The interaction of plasmids with the permeabilized membrane would be thus a fast process (about a hundred microseconds). The plasmid/membrane complexes are stabilized in a delay of 200 ms. A distinct role from the intensity of the electric field and the number of electric pulses was highlighted. If the intensity of the electric field defines membrane surface where the interaction of the plasmid molecules takes place and in fact, the number of spots of interaction, the number of electric pulses defines the amount of plasmids presents by complex. The plasmid/membrane complexes thus formed do not diffuse laterally in the membrane. The actine cytoskeleton is not involved in the formation of these complexes but could be involved in the intracellular traffic of plasmids. Electropermeabilization and plasmid/membrane interaction disturbed the lateral mobility of membrane proteins of outer leaflet of plasma membrane. The combination of the sonoporation with the electropermeabilization makes it possible to improve the effectiveness of transfection obtained by the electropermeabilization alone. The transfer of plasmids by electro-sonoporation is a promising strategy in gene therapy
Lossaint, Gérald. "Mécanismes orchestrant la sortie du cycle cellulaire opérant en G2." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20040/document.
Cancer is a multi-step process resulting from abrogation of several barriers to uncontrolled proliferation. They include inhibitory pathways with appropriate checkpoints that lead to reversible (quiescence) or irreversible (senescence, apoptosis) block of cell proliferation. We are especially interested in pathways orchestrating cell cycle exit that operate in the G2 phase. The first objective of this thesis was to decipher mechanisms that prevent mitosis in response to DNA damage. We found that Cdk inhibitor p21Waf1 plays a crucial role in blocking mitotic onset in normal cells; acting in tandem with checkpoint kinase Chk1, p21 inactivates mitotic Cdks and inhibits pRb phosphorylation, thereby irreversibly blocking mitotic entry. In contrast, in p53-proficient transformed cells, the induction of p21 in G2 is impaired, most likely because of deficient ATM activation. While, in some cases, Chk1 hyper-activation prevents mitosis, the absence of p21 compromises the senescence program from G2. Finally, we showed that Chk2 is dispensable for G2 arrest in both non-transformed and transformed cells (Lossaint et al., submitted). Our second objective was to elucidate the pathways that induce quiescence (G0). This reversible cell cycle exit occurs in G1, requires pRb family members and p27Kip1-dependent Cdk inactivation. Based on observations obtained in our team and the data in the literature, we hypothesized that reversible cell cycle exit program might be launched before mitosis. By using an in vitro wounding model, we showed that confluence-driven quiescence is preceded by pre-mitotic CDK inhibition by p27, cyclin D1 downregulation and reduced pre-mitotic pRb phosphorylation (Chassot et al., 2008). Moreover, our results obtained in synchronized fibroblasts that were serum-starved after release from G1/S block suggest that cyclin D1 might stimulate proliferation by keeping pocket proteins phosphorylated during G2/M progression (Lossaint et al., in preparation)
Khemaissa, Sonia. "Mécanismes d'interaction membranaire et de pénétration cellulaire de peptides vecteurs." Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS659.pdf.
CPPs (Cell Penetrating Peptides) are peptides with cell penetration and transport faculties. These peptides, containing less than 30 amino acids, are generally cationic due to the high occurrence of basic residues and sometimes amphipatic. However, this internalization is non-selective, whatever the cell line. There are two main mechanisms for CPPs uptake: endocytosis and translocation. Endocytosis relies on cellular machinery, while translocation involves transient disruption of the lipid bilayer. Whatever the route of entry, the first step in the internalization process is always an interaction with membrane partners on the cell surface, namely lipids and glycosaminoglycans (GAGs). However, the mechanism of CPP internalization is the subject of much debate in the scientific community. The aim of this thesis was to provide keys for a better understanding of the internalization mechanism. The first step was to study the involvement of GAGs in the internalization mechanism. To investigate this point, chimeric peptides containing a GAG recognition sequence and a CPP sequence were designed. Quantification of internalization was carried out in different cell lines with variations in GAG composition and proportion. The contribution of Trp to CPP interactions was also investigated. To do so, the three Trp residues in the RW9 sequence (RRWWRRWRR-NH2) were substituted by other amino acids or by Trp analogues with different physico-chemical properties. Finally, the last part of this thesis focused on the development of new techniques for cytosolic CPPs quantification at physiological temperature, based on the complementation of luminescent proteins
Dos, Santos Ferreira Jorge. "Identification des mécanismes en boucle fermée dans le comportement cellulaire." Compiègne, 2008. http://www.theses.fr/2008COMP1734.
The aim of this work is to try to use observed global changes to understand interactions between individual nodes inside biochemical networks. We have worked on the determination of the essential interactions in the auto regulatory process that describes the cell cycle of Xenopus frog eggs. The results make possible an assessment of the effect of each protein on the biochemical network stability. The technique was applied also to a dynamical analysis of a uterine cell electrical activity model with view to study the impact of physiological parameters on the response of the model and identify the main subsystems generating the electrical activity. We also present a model developed for understanding an enzymatic diffusion-reaction system. The objective is to analyze the dynamic behavior of three different chemical species, the modification of enzymatic kinetic properties and the existence of sophisticated behaviors resulting of the catalytic activity induced by immobilization of Acetylcholinesterase enzyme into an artificial membrane enzymatically inactive. The results make possible the characterization and prediction of system behavior as well as a qualitative analysis of the system stability via bifurcation diagrams. The model is then extrapolated to a distributed system in order to analyze its spatio-temporal behavior. Numerical results make possible the assessment of the concentration profile of the chemical species on space and time, what is not directly observable by biochemists. Finally, we study a model developed for a network of Sinorhizobium meliloti bacterium and propose an algorithm for intracellular fluxes estimation
Walid, Medhioub. "Étude des mécanismes de contamination des mollusques bivalves par des neurotoxines à action rapide (FAT) & développement de procédés de détoxification." Phd thesis, Université de Bretagne occidentale - Brest, 2011. http://tel.archives-ouvertes.fr/tel-00598247.
Medhioub, Walid. "Étude des mécanismes de contamination des mollusques bivalves par des neurotoxines à action rapide (FAT) & développement des procédés de détoxification." Brest, 2011. http://www.theses.fr/2011BRES2008.
This study aimed to determine the optimal conditions of growth and toxin production in Karenia selliformis and Alexandrium ostenfeldii in order to produce cells at a high concentration with known toxicity to perform further contamination and detoxification trial on edible shellfish, Moreover, this work aims to study the impact of non-toxic microalga on the detoxification kinetics of clam Ruditapes decussatus contaminated by gymnodimines anti oyster Crassostrea gigas contaminated by spirolides. The final goal of this study is to determine the physiological impact of toxic microalgae in the shellfish tissues. Initially, results revealed that the growth performance of K. Selliformis (growth rate and maximum concentration) is obtained at a temperature of 22°C and at a salinity of 36 psu when using the f/2 medium, while those of A. Ostenfeldii are obtained at a temperature of 16°C and at a salinity of 35 psu using the L1 medium. Gymnodimine concentration increases with the age of the culture of K. Selliformis while spirolide concentration decreases during cell growth of A. Ostenfeldii especially during the culture in a photobioreactor of 100l. Secondly, the experimental studies focused on the interaction between toxic micro-algae with molluscs bivalves. The results revealed i) a major accumulation of GYMs and SPXs in digestive gland of clams and oysters ii) a rapid detoxification of contaminated shellfish when adding food. Finally, this study addressed an important issue on the impact of toxic algae on shellfish. The exposure to A. Ostenfeldii showed i) a decrease in the digestive gland tubule thickness and the percentage of active digestive tubules ii) an inflammatory response consisting of hemocyte infiltration and diapedesis into the intestinal tract of the oysters. Concerning the natural and experimental clams, histological analysis did net reveal any alteration of the digestive gland as demonstrated in oysters contained by A. Ostenfeldii
Частини книг з теми "Mécanismes de détoxification cellulaire":
COSTANTINI, Lindsey M., and Blossom DAMANIA. "Virus à ADN." In Virologie, 7–37. ISTE Group, 2022. http://dx.doi.org/10.51926/iste.9023.ch1.