Dissertations / Theses on the topic 'Mécanismes de détoxification cellulaire'
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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
Dransart, Estelle. "Mécanismes moléculaires des rhoGDIs : le système rhoGDI3/RhoG/TrioGEF comme modèle d'nvestigation." Paris 11, 2005. http://www.theses.fr/2005PA112108.
Zeltz, Cédric. "Analyse des mécanismes d'interaction du lumicanne avec les cellules." Reims, 2009. http://www.theses.fr/2009REIMM205.
@Lumican is an extracellular matrix leucine-rich protein. We previously showed that lumican inhibited melanoma progression in vivo (Vuillermoz et al. 2004). In the present study, we have characterized the mechanisms involved in the anti-migratory effect of lumican. We identified the alpha2beta1 integrin as a lumican receptor to mediate the inhibitory effect of lumican on cell migration. Moreover, we provide evidence of a direct binding of lumican to the alpha2beta1 integrin and the I domain of the alpha2 integrin subunit (Kd=300 nm). In a second time, we localized the active sequence responsible of migration inhibition in the leucine-rich repeat 9 of lumican. We proposed the name lumcorin (fragment of lumican core protein) for the peptide derived from this site. Lumcorin inhibited melanoma cell migration and FAK phosphorylation, as previously observed for lumican (Brézillon et al. 2009). Furthermore, the lysine located in lumcorin and corresponding to the lysine 265 and 267 of lumican, seemed to be necessary to induce the migration inhibition. Lumican and lumcorin inhibited the migration of nontransformed cells such as dermal fibroblast, suggesting a regulator role of these molecules in cell migration involved in physiological processes different to cancer
Dessauge, Frédéric. "Etude des mécanismes de mort cellulaire programmée dans les cellules transformées." Paris 7, 2004. http://www.theses.fr/2004PA077052.
Jourdan, Eric. "Mécanismes de protection cellulaire endogène et exogène suite à l'irradiation ultraviolette." Université Joseph Fourier (Grenoble), 2002. http://www.theses.fr/2002GRE18005.
We studied two important photoprotection mechanisms, endogenous zinc dependant photoprotection and exogenous photoprotection ensured by sunscreens. Firstly our work demonstrates the protective role of zinc treatment against oxidative stress in HeLa cells. We showed that metallothioneins were strongly expressed in zinc treated cells. Then a great protection against DNA oxidative damages and cell death was observed. The induction of metallothioneins, i. E. Small cystein rich proteins, seems to represent the main way for zinc to afford protection against oxidative cellular damages. Secondly we demonstrated the protective role of zinc on keratinocytes exposed to solar light. The genoprotection afforded by zinc treatment was inductible and correlated to the time of zinc treatment. The nuclear redistribution of MTs indicates the important role of these proteins in the protection of the genome after a solar irradiation. We showed that only Zn-metallothioneins could afford genoprotection. After irradiation, the intracellular amount of MTs decreased, probably due to the protein oxidation by irradiation induced ROS. As a consequence MTs released zinc atoms which could stimulate the activity of nuclear zinc proteins such as XPA. Moreover the intracellular MTs degradation could modulate the nuclear redox potential and consequently the Ref-1 protein activity. Our results on XPA and Ref-1 show that zinc treatment modulates the expression of these two DNA repair enzymes. These results underline the interrelation between zinc, MTs, and DNA repair systems in maintaining genomic integrity. Our study concerning exogenous photoprotection induced by sunscreens demonstrates the importance of new biomarkers to assess the real photoprotective profile of a sunscreen in addition to SPF determination. These important biomarkers (CPF, GPF, APF, EPF), evaluated in vitro, could be considered as important parameters to evaluate the long term photoprotective capacity of sunscreens as they take in account both UVB and UVA deleterious effects
Mokas, Sophie. "Mécanismes d'assemblage des granules de stress." Thesis, Université Laval, 2012. http://www.theses.ulaval.ca/2012/28583/28583.pdf.
Rouas, Caroline. "Etude des mécanismes mis en jeu lors d'une exposition à l'uranium appauvri sur le système de détoxification in vivo et in vitro." Paris 11, 2010. http://www.theses.fr/2010PA114835.
The aim of this work is to study the effects of a uranium (U) exposure on organs involved in the detoxification: the kidney and the liver (and notably the xenobiotics metabolizing enzymes (XME)). In order to mimic population chronic exposure, rats were contaminated during 9 months through drinking water (40 mg/L). In vivo results show that U exposure does not induce neither nephrotoxicity nor sensitivity to increase a renal toxicity induced by gentamicin. In the liver, U provokes impairments on the XME gene expression. Nevertheless, paracetamol metabolism is modified only if it is administrated at a hepatotoxic dose. The in vitro results suggest an indirect effect of uranium on the XME, probably dependant of body adaptation mechanisms. Besides, in vitro studies underlined cytotoxic properties of U as well as the localisation of its soluble and/or precipited forms in cytoplasmic and nuclear compartments
Igel, Angélique. "Mécanismes d'inactivation des protéines amyloïdes." Paris 7, 2013. http://www.theses.fr/2013PA077101.
Amyloides fibers correspond to insoluble protein assemblies associated to the neurodegenerative diseases. By taking into account properties biophysics of these fibers which confer them a very high resistance, and the spectre of their transmissibility, everything lets suggest that medical surgical acts could potentially lead or transmit amyloidoses by the inoculation of nucleation seed. The objective of this work is to estimate mechanisms of inactivation of A ß and prion assemblies, to understand the mechanisms of inactivation of amyloides proteins. At first, we estimated the evolution of the quaternary structure of the assemblies of prion stemming from 3 strains (263K, vCJD and 139A) after decontamination treatments. Ail results demonstrate that the inactivation of prion are strain dependent. This intrinsic property of strain would be due to different structuring of PrP protomers within the assemblies. Finally, similar approaches to those used on the field of prions were used to estimate the résistance of amyloide assemblies stemming from the Alzheimer's disease (peptide A ß). Our preliminary results of synthetic peptide A ß inactivation, show that this peptide, in its fibrillar state, possesses properties conferring it a high strength. To deepenour results in a model of peptide having sudden a maturation of in-vivo withdrawal, we have designed a new cellular model expressing the peptide A640. This new tool is operational recently and seems promising for the study of the properties of the peptide Aß
Alegot, Hervé. "Etude des mécanismes d'élongation du follicule ovarien de Drosophila melanogaster." Thesis, Clermont-Ferrand 1, 2016. http://www.theses.fr/2016CLF1MM06/document.
Tissue elongation plays a key role during development. Schematically, this morphogenetic process can be described by three main parameters: the cue orienting the elongation, the movement generating force and the associated cellular behavior. The Drosophila ovarian follicle, initially spherical, elongates as it develops, ending as a 2.5 time longer than wide mature egg. I found that follicles elongate through at least three consecutive phases and I aimed to determine the parameters of the early phase. The signal comes from a cluster of cells located at each pole of the follicle secreting the Jak-Stat pathway ligand and the subsequent activation of the pathway as a gradient from the poles. A pulling force is generated by the Jak-Stat dependent apical pulsations of the cells following the same gradient. The elongation is stabilized by oriented cell intercalations along the elongation axis and a gradient of apical constriction. Our data allow proposing a mechanism where a gradient of transcription factor activity can lead to epithelial elongation without any planar polarity requirement
Schlemmer, Frédéric. "Mécanismes de la chimiothérapie immunogène." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T075.
The steady improvement of cancer prognosis is the result of progress in cancer prevention, screening, diagnosis and treatment. Despite the recent advent of targeted therapies, conventional chemotherapy often remains the only solution for patients with non-operable cancer or not eligible for these novel therapies.Some conventional chemotherapy (including anthracyclines and oxaliplatin) has the ability to cause tumor cells death with characteristics able to induce an effective antitumor immune response. This specific antitumor immune response would be synergistic with the direct cytotoxic effect of these drugs and contribute to their efficacy. The antitumor immune response induced by chemotherapy depends on several key cellular and molecular mechanisms recently identified. The induction of an endoplasmic reticulum (ER) stress is necessary for the exposure of calreticulin (CRT), an ER-resident chaperone protein, on the surface of dying cells, then acting as a phagocytosis signal for dendritic cells. Release of danger signals into the extracellular medium is also essential. The nuclear protein High Mobility Group Box 1 (HMGB1) is a ligand of the Toll-like receptor 4 (TLR4) on the surface of dendritic cells. TLR4 activation promotes the processing of tumor antigens and their presentation to cytotoxic T lymphocytes. Adenosine-5'-triphosphate (ATP) is also released by tumor cells, leading to the activation of the purinergic receptors P2RX7 expressed on the surface of dendritic cells, activating the NLRP3 inflammasome and causing the release of IL-1β by dendritic cells, while promoting the orientation of the immune response towards a TH1 response and the production of γ-interferon by cytotoxic T lymphocytes.In this work, we aimed to compare the ability of two drugs of a same class of chemotherapy, the platinum derivates oxaliplatin (OXP) and cisplatin (CDDP), to induce immunogenic death of tumor cells. Thanks to in vitro and in vivo experiments (models of tumor vaccination and chemotherapy on established tumors in mice), we showed that OXP, in contrast to CDDP, has the ability to induce immunogenic death of colon cancer cells. This intra-class difference depends on the ability of each drug to cause one of the key phenomena of immunogenic cell death: the induction of the exposure of the CRT to the surface of dying tumor cells. We could also show that the induction of immunogenic death of colon cancer cells by OXP had clinical relevance in humans. Indeed, the existence of a loss-of-function polymorphism of tlr4 affects the prognosis (PFS) of patients treated with OXP-based chemotherapy regimen for a metastatic colorectal cancer. Subsequently, we developed biosensors to study the ability of different drugs to induce key phenomena of cell death immunogen tumor cells (CRT exposure, HMGB1 and ATP release) using high-content screening by an automated video-microscopy platform. We showed that a pharmaceutical correction of the inability of cisplatin to induce an endoplasmic reticulum stress could restore the immunogenicity of cisplatin-induced tumor cell death. These results open the way to the discovery of new molecules that, alone or in combination with other known therapies, could improve the prognosis of cancer
Cueille, Nathalie. "Etude des mécanismes de contrôle de la réplication des papillomavirus." Montpellier 1, 1999. http://www.theses.fr/1999MON1T016.
El, hallani Soufiane. "Nouveaux mécanismes alternatifs de la vascularisation tumorale dans les glioblastomes." Paris 11, 2009. http://www.theses.fr/2009PA11T063.
Tardy, Magalie. "Étude des mécanismes de régulation des canaux potassiques à deux domaines P." Nice, 2010. http://www.theses.fr/2010NICE4020.
Potassium channels form the most diverse class of ion channel family. Three families of potassium channels have been identified, including the two P domain potassium channel family. This family is the last one identified and counts 15 members. These channels produce leak currents that play a key role in cellular excitability, and more particularly in seizures, anesthesia, neuroprotection or depression. A detailed study of the mechanisms regulating the channel activity is necessary for a better comprehension of their roles. We studied the protein environment of the TREK1 channel and we showed that a cytosolic protein associated to microtubules, Mtap2, is able to bind TREK1. This association leads to an increase of TREK1 expression at the plasma membrane. This protein is the second identified. Both of them can bind TREK1 simultaneously and have additive effects, placing TREK1 at the center of a protein network. These results show how much the protein environment of channels is important for their activity. We also showed that TWIK1 is localized in a subapical compartment near the plasma membrane. TWIK1 is actually inserted in the membrane then quickly internalized and addressed to the recycling endosomes. The export from this compartment is drived by activation of a Gi coupled receptor. This activation could be the physiological signal leading to an increase of TWIK1 currents at the plasma membrane
Deluche, Cynthia. "Endoréduplication, division et expansion cellulaire : mécanismes acteurs de la croissance du fruit." Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0199/document.
The transformation of the ovary wall into a fleshy pericarp involves a coordinated pattern of cell division and cell expansion. Considerable data have been reported on tomato fruit development and ripening, but the pattern of cell division, cell expansion and endoreduplication at the tomato fruit set and during fruit growth remains grossly appreciated at the whole pericarp level and many questions are not yet resolved: How are cell division and cell expansion coordinated in tomato fruit a cellular level and according to developmental time? When does endoreduplication begin in fruit tissues and what is its function? The first part of this deals with the coordination of cell division and cell expansion during the end of tomato ovary development and the beginning of fruit growth. Evidence for early differentiation of cell layers in the ovary wall and then in fruit pericarp are presented. Cell division happens mainly in the external epidermis and shows partial synchronization, whereas cell expansion happens mostly in mesocarp cell layers. Endoreduplication is initiated as soon as before anthesis. The second part of this work is devoted to RNA-seq based transcriptome profiling of pericarp nuclei which have been sorted according to four ploidy levels (4, 8, 16 and 32C). We demonstrate that the expression of most of the pericarp-expressed genes shows a proportional increase according to ploidy level, on a nuclear basis. However, a significant amount of genes has been identified as over-expressed or under-expressed according to ploidy level
Daouphars, Mikaël. "Mécanismes d'action des AINS en relation avec la prolifération cellulaire et l'apoptose." Nancy 1, 2004. http://docnum.univ-lorraine.fr/public/SCD_T_2004_0258_DAOUPHARS.pdf.
Fernet, Marie. "Etude des mécanismes impliqués dans la réponse cellulaire précoce aux radiations ionisantes." Paris 11, 2000. http://www.theses.fr/2000PA11T063.
Lévesque, Tremblay Véronique. "Mécanismes d'action de CRB3 dans le contrôle de la croissance tumorale." Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27008/27008.pdf.
Lin, Thibault. "Mécanismes du transfert intercellulaire des homéoprotéines." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066346/document.
Homeoproteins belong to a family of transcription factors which all share a common DNA binding domain, the homeodomain. Beside their action as transcription factors, homeoproteins are also able to be transferred between cells by unconventional means. The two consecutive steps of this intercellular transfer (secretion then internalisation) require sequences located in the homeodomain. Thanks to studies previously lead by our laboratory, we know that subcellular localisation of ENGRAILED-2 (EN-2) homeoprotein is a crucial step in its subsequent secretion. On this basis, we showed that EN-2 interacts directly with a certain subtype of phospholipids, phosphoinositides [e.g. PI(4,5)P2]. Then, we demonstrated than these lipids are involved in the association of EN-2 protein with membraneous compartments within the cell. PI(4,5)P2 located in the inner leaflet of the plasma membrane are also involved in the direct translocation of EN-2 across plasma membrane. This work is also focused on the role of proteoglycans, and more precisely syndecans, in EN-2 cell surface accumulation after both secretion and internalisation. At last, we also established the implication of EN-2 interaction domain with PBX in EN-2 intercellular transfer
D'Onofrio, Marie-France. "Etude in vitro de mécanismes anti-tumoraux induits par le lumicanne recombinant sur les cellules de mélanome." Reims, 2008. http://www.theses.fr/2008REIMM201.
Combe, Christian. "Les mécanismes de l'adhésion leucocytaire : implications en néphrologie." Bordeaux 2, 1995. http://www.theses.fr/1995BOR28330.
Mediouni, Chamseddine. "Analyse des voies de détoxification des métaux lourds chez les plantes et lien avec les réponses cellulaire et moléculaire après traitement aux agents génotoxiques." Strasbourg, 2009. http://www.theses.fr/2009STRA6213.
This work presents the response of plants [tomato, Arabidopsis thaliana Col0 and A. Thaliana cad2 mutant, defective in the glutathione (GSH) biosynthesis pathway] to heavy metal excess. At the physiological level, the treatment with cadmium or copper induce plant growth inhibition, more pronounced at high copper concentration. Differences in heavy metal toxicity could be linked to variation of heavy metal tolerance mechanisms like phytochelatine chelation. At the biochemical level, the two heavy metals induce oxidative stress. In response to ROS accumulation, there is an increase of antioxydative enzyme activity in the leaves of wild type plants, whereas, the lack of GSH biosynthesis leads to the lack of antioxydative response in the cad2 mutant. At the molecular level, cadmium and copper induce, essentially via ROS accumulation, DNA double strand break (DSBs) in the leaves of Arabidopsis thaliana Col0 and of the mutant cad2 and cell death in the leaves and the roots of both plant types, characterized by an induction of specific gene expression. On the other hand, a high induction of cell death is related to a great accumulation of DSBs and the lack of repair gene induction. This suggests that cells are directed towards cell death rather than to DNA repair if DNA damages are to much accentuated
Plawinski, Laurent. "Nouveaux mécanismes fibrinolytiques des nanovésicules cellulaires : Détection et relevance physiopathologique." Paris 7, 2012. http://www.theses.fr/2012PA077013.
This thesis is based on a set of three fundamental articles and a review on the fibrinolytic activity of nanovesicles presenting as new concept: the fibrinolytic cross-talk. A patent on a new methodology to separate specifically the nanovesicles from the other nanoobjects present in human biological fluids has been obtained from the INPI on March 23rd, 2011 (patent registration n°l 1/00873). The objective of the first article was to demonstrate in vitro that endothelial derived-nanovesicles from human dermal microvascular endothelial cells (HMEC), carry on their surface the complex uPA/uPAR and that they act as catalytic surfaces capable of interacting with plasminogen to generate plasmin. In the second article we demonstrate the proof of concept that fibrinolytic nanovesicles are present in circulating human blood. We also show that plasminogen activators are distinctly borne by nanovesicles of specific cell origin: endothelial nanovesicles bear tPA whereas nanovesicles of leukocyte origin bear uPA. The third article concerns the existence of a new mechanism of plasmin generation: the fibrinolytic cross-talk. This mechanism raises two requirements: first the nanovesicle must bear uPA; second, plasminogen must be hold by a different surface (fibrin, membrane cells or extracellular matrix). Finally, a review close this subject by synthesizing all these studies and ends by the perspectives which they offer to the field of cellular fibrinolytic nanovesicles
Lin, Thibault. "Mécanismes du transfert intercellulaire des homéoprotéines." Electronic Thesis or Diss., Paris 6, 2015. http://www.theses.fr/2015PA066346.
Homeoproteins belong to a family of transcription factors which all share a common DNA binding domain, the homeodomain. Beside their action as transcription factors, homeoproteins are also able to be transferred between cells by unconventional means. The two consecutive steps of this intercellular transfer (secretion then internalisation) require sequences located in the homeodomain. Thanks to studies previously lead by our laboratory, we know that subcellular localisation of ENGRAILED-2 (EN-2) homeoprotein is a crucial step in its subsequent secretion. On this basis, we showed that EN-2 interacts directly with a certain subtype of phospholipids, phosphoinositides [e.g. PI(4,5)P2]. Then, we demonstrated than these lipids are involved in the association of EN-2 protein with membraneous compartments within the cell. PI(4,5)P2 located in the inner leaflet of the plasma membrane are also involved in the direct translocation of EN-2 across plasma membrane. This work is also focused on the role of proteoglycans, and more precisely syndecans, in EN-2 cell surface accumulation after both secretion and internalisation. At last, we also established the implication of EN-2 interaction domain with PBX in EN-2 intercellular transfer
Lassus, Patrice. "Etude des mécanismes de contrôle de l'apoptose par le gène suppresseur de tumeurs p53." Montpellier 2, 1998. http://www.theses.fr/1998MON20164.
Kolli, Kaouther. "Rôle de la protéine FAK (Focal Adhésion Kinase) dans les mécanismes d'invasion cellulaire." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ003.
This thesis is about the role of the protein FAK (Focal Adhesion Kinase) in the cellular mechanisms of invasion
Reix, Stéphanie. "Ré-évaluation des mécanismes de mort cellulaire programmée associée à la maladie d'Alzheimer." Aix-Marseille 2, 2006. http://theses.univ-amu.fr.lama.univ-amu.fr/2006AIX22086.pdf.
Orré, Thomas. "Mécanismes moléculaires d’activation des intégrines par la kindline-2 lors de l’adhésion cellulaire." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0824/document.
Focal adhesions (FAs) are adhesive structures linking the cell to the extracellular matrix (ECM) and constitute molecular platforms for biochemical and mechanical signals controlling cell adhesion, migration, differentiation and survival. Integrin transmembrane receptors are core components of FAs, connecting the ECM to the actin cytoskeleton. During the early 2000s, the intracellular protein talin, which directly binds to the cytoplasmic tail of β-integrins, was considered as the main integrin activator. Nevertheless, it has been shown that kindlin, another intracellular protein that bind to β-integrin, is also a critical integrin activator. In fact, several studies have shown that kindlin and talin play complementary and synergistic roles during integrin activation. The molecular basis of these phenomena remains to determine. Moreover, most studies focusing on the role of kindlin during integrin activation and cell adhesion have been performed with suspended cells and/or with the platelet integrin αIIbβ3. Here we combined PALM microscopy with single protein tracking to decipher the role and behavior of kindlin during key molecular events occurring outside and inside FAs at the plasma membrane and leading to integrin activation, as we have done previously for talin (Rossier et al., 2012). We found that beta1 and beta3-integrins with a point mutation inhibiting binding to kindlin show reduced immobilization inside FAs. We also found that kindlin-2, which is enriched inside FAs, displayed free diffusion at the plasma membrane outside and inside FAs. This constitutes a major difference with talin, which, at the plasma membrane level, is observed almost exclusively in FAs, where it is immobile, which shows that talin is recruited into FAs directly from the cytosol without lateral diffusion along the plasma membrane (Rossier et al. 2012). To determine the molecular basis of kindlin membrane recruitment and diffusion, we used a kindlin variant known to decrease binding to integrins (kindlin-2- QW614/615AA). This mutant displayed increased membrane diffusion, suggesting that kindlin-2 can freely diffuse at the plasma membrane without interacting with integrins. Moreover, the kindlin-2-QW mutant showed decreased immobilization inside FA, showing that part of kindlin immobilization depends on interaction with integrins. This suggests that kindlin can form an immobile complex with integrins inside focal adhesions. Deletion of the kindlin pleckstrin homology (PH) domain strongly reduced the membrane recruitment and diffusion of kindlin. We assessed the functional role of kindlin membrane recruitment and diffusion by re-expressing different kindlin-2 mutants in kindlin-1/kindlin-2 double KO cells. Those experiments demonstrated that kindlin-2 membrane recruitment and diffusion are crucial for integrin activation during cell spreading and favor adhesion formation. This suggests that kindlin uses a different route from talin to reach integrins and trigger their activation, providing a possible molecular basis for their complementarity during integrin activation
Dakhli, Haithem. "Mécanismes d'induction du cannibalisme cellulaire et conséquences sur la réponse aux traitements anticancéreux." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS585.
Cannibalism of live cells by other live cells is a new modality of non-autonomous cell death. This investigation led to the characterization of the molecular mechanisms implicated as well as the identification of the consequences of this process on the fate of the cannibal cell.We revealed that the activation of a signaling pathway involved in the regulation of the cell cycle can trigger a release of ATP that will stimulate the activity of the P2Y2 purinergic receptor in an autocrine manner. These events will lead to the increase of E-cadherin membrane exposition and change the organisation of the cytoskeleton in a ROCK-dependent manner, allowing this live cell to eat another live cell. This process called "cell in cell structure" is frequently observed in tumoral biopsies. Then, we revealed that the internalized cell will be eliminated by a process dependent on the autophagy protein ATG5 and the pro-apoptotic proteins BAX and BAK. These events are associated to the triggering of genomic instability and an oxidative stress in the cannibal cell leading these cells to a new senescence program that we called "entescence".This new senescence program seems to be a tumor suppressor mechanisms in vivo and is correlated to a better response of patient to neoadjuvant anticancer treatments. Moreover, escaping entescence seems to favor tumor growth and is associated to a bad response to anticancer treatments.Taken together, these results highlight the existence of a new senescence program that is initiated by cellular cannibalism. A better understanding of the molecular mechanisms regulating its initiation and its execution may lead to develop new innovative anticancer therapeutical approaches
Ezan, Jérôme. "Etude des propriétés angiogéniques de FrzA : mécanismes moléculaires impliqués." Bordeaux 2, 2005. http://www.theses.fr/2005BOR21196.
FrzA is a secreted Frizzled Related Protein (sFRP) thought to interfere with the Wn/tFrizzled pathway. This protein is expressed in the cardiovascular system, has antiproliferative effect on vascular cells, induces endothelial cells (EC) migration in vitro and has proangiogenic effects in vivo. In this work, we aimed to study cellular and molecular mechanisms allowing FrzA to exert its effects. Using in vitro and in vivo (hindlimb ischemia mouse model) studies, we demonstrated that FrzA delays G1 phase and entry into S phase. This delay is associated with a decrease in the level of cyclin D1/E and Cdk 2/4. Our results showed that FrzA promotes EC spreading, a prerequisite to migration, through integrin αβ1 in vitro. This spreading requires GSK3β and GTPase Rac1 activation and might involve Frizzled receptors
Siaussat, David. "Mécanismes moléculaires impliqués dans le contrôle de la prolifération cellulaire par les ecdysteroïdes chez le Lépidoptère Plodia interpunctella." Paris 6, 2004. http://www.theses.fr/2004PA066303.
Nègre, Paulin. "Mécanismes de motilité et guidage sous flux des leucocytes humains." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0747/document.
A fast and efficient immunity response needs leukocytes’ability to migrate within the entire organism. Their migration, called amoeboid, is characterized by a high speed (10-20 μm.min-1) and a great adaptability to move through various environment, either two-dimensional as luminal endothelial surface or tri-dimensional (3D) environment as tissue. Since the observation of leukocytes migrating without adhesion through solid 3D medium, amoeboid migration is described as requiring either adhesion or friction with solid support to permit motility. We showed here that effector T lymphocytes are able to swim without any interaction with solid substrate. Propulsion is based on actin retrograde flow coupled with transmembrane proteins linked to cytoskeleton (like integrins) which drag a brush of polymeric molecules in interaction with the medium. Furthermore, cell guidance is required for many crucial functions as organism growth or immune system. However, when crawling on luminal endothelial surfaces, cells are exposed to blood flow and they robustly orient either with or against the flow with unknown mechanisms. We showed that lymphocytes and neutrophils flow orientation can be explain without any molecular flow sensor of shear stress. Lamellipodium for neutrophils and uropod for lymphocytes is non-adherent and orients in the direction of flow like a wind vane. Front-rear cell polarization aligns the axis of the whole cell with the non-adherent pole oriented by flow. Flow mechanotaxis of leukocytes relies on passive mechanisms without mechanotransduction
Sabatier, Nancy. "Mécanismes subcellulaires de l'autocontole des neurones vasopressinergiques magnocellulaires chez le rat." Montpellier 2, 1999. http://www.theses.fr/1999MON20105.
Avril, Tony. "Etude des mécanismes de résistance des cellules trophoblastiques à la cytotoxicité naturelle." Tours, 2000. http://www.theses.fr/2000TOUR4007.
No summary available
Coulbault, Laurent. "Mécanismes impliqués dans la régulation des MAP kinases par les récepteurs opioïdes delta." Caen, 2008. http://www.theses.fr/2008CAEN3010.
Opioid receptor desensitization, endocytosis, and cellular trafficking may play an important role in the development of opiate tolerance. Previous studies in our laboratory showed an agonist dependent regulation of human delta opioid (hDOP) receptor observed on cAMP pathway desensitisation and receptor endocytosis. In this work, we studied the effect of selective (DPDPE, deltorphin I, UFP-512) and non-selective (etorphine, morphine) agonists on Mitogen-Activated Protein Kinases pathways in SK-N-BE cell line. Our major findings are summarized as follows: selective and non-selective agonists activate Extracellular signal-Regulated protein Kinases ERK1/2 by similar pathways; as previously demonstrated on the cAMP pathway, chemical structure of agonists affects hDOP receptor desensitization on ERK1/2; ERK1/2 are not involved in the regulation of hDOP receptor endocytosis; a differential hDOP receptor regulation (internalization and desensitization on cAMP pathway) by β-arrestin 1 upon selective and non-selective opioid agonists exposure, our results suggest that β-arrestin 1 can interact with two sites on hDOP receptor producing either desensitisation or internalisation, β-arrestins and hDOP endocytosis are not involved in ERK1/2 activation with opioïd agonists; we demonstrate a link between the propensity of an opioid agonist, UFP-512, to produce a weak desensitization on adenylyl cyclase and ERK1/2 pathways, a strong hDOP endocytosis associated with a significant recycling, and the absence of tolerance in vivo
Bernis, Cyril. "Caractérisation de nouveaux mécanismes de régulation de la kinase mitotique Cdk1-cycline B." Montpellier 2, 2007. http://www.theses.fr/2007MON20246.
Michel, Virginie. "Les mécanismes de la vulnérabilité à la chaleur : implication des stress systémique et cellulaire." Phd thesis, Université Claude Bernard - Lyon I, 2007. http://tel.archives-ouvertes.fr/tel-00203725.
Guez, Fanny. "Etude des mécanismes moléculaires impliqués dans le cycle cellulaire des cellules β pancréatiques humaines." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T094.
Diabetes is a disease that affects 347 million people worldwide (90% with type 2 diabetes) (WHO, September 2012). It is defined by a disturbance in the regulation of glucose homeostasis with a deficit in function of pancreatic beta cells. In type 1 diabetes, this deficit is caused by autoimmune destruction. In type 2 diabetes, it is due to peripheral insulin resistance leading to a depletion of beta cells that can no longer maintain their function. A strategy to restore a functional beta cell mass is, or of inducing proliferation of these cells in vitro prior to transplant, or to induce proliferation in vivo. However, this implies a better understanding of the molecular mechanisms involved in the cell cycle of human pancreatic beta cells. The aim of my thesis was to dissect these mechanisms. For this, we have a unique laboratory tool, two lines of human pancreatic beta cells. In one of them, immortalizing transgenes may be deleted. Then, the cells stop to proliferate giving pseudo- primary beta-cells. By comparing the expression of cell cycle regulators of the lineage of human beta cells immortalized pseudo- primary human beta- cells, we could show that the cycle of these cells was blocked in the G1 phase. The lack of several proteins responsible for cell cycle progression downstream of this phase has been confirmed in human islets. We also observed a decrease in the doubling time of human beta cells following treatment with GH and EPO. Following this treatment we also observe an activation of the transcription factor STAT5 known for its involvement in cell proliferation of rodent beta cells. Finally, we studied the effect that caused a nutrient supply on the function and proliferation of human beta cells. We have seen that the cells responded better to beta function with a doubling time shorter amount of cells in a nutrient enriched environment. In addition, under these conditions, autophagy, existing before the supply of nutrients and likely due to a lack of cellular energy, disappears. These results allow us to better understand the mechanisms controlling proliferation of human pancreatic ß and consider new diabetes therapies cells
Heitzler, Domitille. "Modélisation dynamique des mécanismes de signalisation cellulaire induits par l'hormone folliculo-stimulante et l'angiotensine." Phd thesis, Université François Rabelais - Tours, 2011. http://tel.archives-ouvertes.fr/tel-00847767.
Morissette, Guillaume. "Séquestration ionique et vacuolisation cellulaire : étude des mécanismes et des répercussions physiologiques et pharmacologiques." Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25646/25646.pdf.
Debard, Virginie. "Les mécanismes de la vulnérabilité à la chaleur : implication des stress systémique et cellulaire." Lyon 1, 2007. http://tel.archives-ouvertes.fr/docs/00/20/37/25/PDF/these_definitif_corrigee.pdf.
Heat stroke is a serious illness without specific treatment. Heat stroked animals exhibit inflammatory processes accompanied by metabolic imbalance. These impairments take place despite of heat shock proteins (Hsp70) induction and glucocorticoid secretion. The role of Hsp70 mRNA and glucocorticoids in heat tolerance has been analyzed. Vigil animals intolerant to heat present: severe hyperthermia and dehydration, metabolic imbalance, lesser glucocorticoid production, signs of cellular hyperactivation and aggression, activation of inflammatory processes. The Hsp70 mRNA expression depends on the intensity of the stressor and appears, in the chain of causality, as a consequence of the heat aggression. Glucocorticoids are involved in tolerance by reducing local inflammatory processes and favouring the expression of the inhibitory factor κBα (IκBα) mRNA
Rosselin, Manon. "Identification et rôle des mécanismes d'invasion cellulaire indépendants du T3SS-1 chez Salmonella Enteritidis." Thesis, Tours, 2011. http://www.theses.fr/2011TOUR4004/document.
The main invasion system of Salmonella requires a type III secretion system (T3SS-1) which promotes a Trigger entry mechanism. However, other invasins were described in Salmonella but their roles in virulence remain unclear. We have shown that Salmonella Enteritidis caninvade cells via the Rck outer membrane protein and we have demonstrated by different approaches that Rck mediates a Zipper entry process. Characterisation of the cellular transduction pathway induced by Rck enable us to propose a model of internalisation involving actin, Arp2/3, Rac and Cdc42, Akt, class I PI3K and Src. Finally, the invasion ability of a S. Enteritidis mutant grown under culture conditions that did not allow the expression of any identified invasion factors (T3SS-1, Rck and PagN) provides evidences for still non-characterised Salmonella invasion factors which seem to induce both Zipper and Trigger mechanisms. Overall, our data indicate that Salmonella is the first bacterium found tobe able to invade cells by both a Trigger mechanism at least mediated by the T3SS-1 and a Zipper entry process at least mediated by Rck. Study of the T3SS-1-independent invasion systems could bring to a better understanding of Salmonella pathogenicity, particularly in regard to the different diseases induced by Salmonella and to its great diversity of hosts