Littérature scientifique sur le sujet « Perméabilisation de la membrane des lysosomes »
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Articles de revues sur le sujet "Perméabilisation de la membrane des lysosomes"
Haylett, T., et L. Thilo. « Limited and selective transfer of plasma membrane glycoproteins to membrane of secondary lysosomes. » Journal of Cell Biology 103, no 4 (1 octobre 1986) : 1249–56. http://dx.doi.org/10.1083/jcb.103.4.1249.
Texte intégralLuzio, J. Paul, Paul R. Pryor, Sally R. Gray, Matthew J. Gratian, Robert C. Piper et Nicholas A. Bright. « Membrane traffic to and from lysosomes. » Biochemical Society Symposia 72 (1 janvier 2005) : 77–86. http://dx.doi.org/10.1042/bss0720077.
Texte intégralAndrews, Norma W. « Lysosomes and the plasma membrane ». Journal of Cell Biology 158, no 3 (29 juillet 2002) : 389–94. http://dx.doi.org/10.1083/jcb.200205110.
Texte intégralGreen, S. A., K. P. Zimmer, G. Griffiths et I. Mellman. « Kinetics of intracellular transport and sorting of lysosomal membrane and plasma membrane proteins. » Journal of Cell Biology 105, no 3 (1 septembre 1987) : 1227–40. http://dx.doi.org/10.1083/jcb.105.3.1227.
Texte intégralToyomura, Takao, Yoshiko Murata, Akitsugu Yamamoto, Toshihiko Oka, Ge-Hong Sun-Wada, Yoh Wada et Masamitsu Futai. « From Lysosomes to the Plasma Membrane ». Journal of Biological Chemistry 278, no 24 (2 avril 2003) : 22023–30. http://dx.doi.org/10.1074/jbc.m302436200.
Texte intégralBlott, Emma J., Giovanna Bossi, Richard Clark, Marketa Zvelebil et Gillian M. Griffiths. « Fas ligand is targeted to secretory lysosomes via a proline-rich domain in its cytoplasmic tail ». Journal of Cell Science 114, no 13 (1 juillet 2001) : 2405–16. http://dx.doi.org/10.1242/jcs.114.13.2405.
Texte intégralJaiswal, Jyoti K., Norma W. Andrews et Sanford M. Simon. « Membrane proximal lysosomes are the major vesicles responsible for calcium-dependent exocytosis in nonsecretory cells ». Journal of Cell Biology 159, no 4 (18 novembre 2002) : 625–35. http://dx.doi.org/10.1083/jcb.200208154.
Texte intégralWAN, Feng-Yi, Yi-Nan WANG et Guo-Jiang ZHANG. « The influence of oxidation of membrane thiol groups on lysosomal proton permeability ». Biochemical Journal 360, no 2 (26 novembre 2001) : 355–62. http://dx.doi.org/10.1042/bj3600355.
Texte intégralRodríguez, Ana, Paul Webster, Javier Ortego et Norma W. Andrews. « Lysosomes Behave as Ca2+-regulated Exocytic Vesicles in Fibroblasts and Epithelial Cells ». Journal of Cell Biology 137, no 1 (7 avril 1997) : 93–104. http://dx.doi.org/10.1083/jcb.137.1.93.
Texte intégralDraye, J. P., P. J. Courtoy, J. Quintart et P. Baudhuin. « A quantitative model of traffic between plasma membrane and secondary lysosomes : evaluation of inflow, lateral diffusion, and degradation. » Journal of Cell Biology 107, no 6 (1 décembre 1988) : 2109–15. http://dx.doi.org/10.1083/jcb.107.6.2109.
Texte intégralThèses sur le sujet "Perméabilisation de la membrane des lysosomes"
Alvarez, Valadez Karla. « Targeting intracellular cholesterol transport for inducing lysosomal damage and immunogenic cell death in cancer ». Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL123.
Texte intégralLysosomes serve as an intracellular platform that coordinates anabolic and catabolic processes, cell signaling, and transcriptional programs. These organelles allow the adaptation of cancer cells to a changing microenvironment by supplying them with essential metabolites and energy for their survival and proliferation. A major player in the lysosomal adaptive response is the transcription factor EB (TFEB), which is part of the microphthalmia/transcription factor E (MIT/TFE) family of transcription factors. TFEB plays a pivotal role in driving the expression of several genes associated with lysosome function and biogenesis, including those participating in autophagy. The latter is a critical lysosomal catabolic process in the cell. While TFEB and autophagy function as adaptive mechanisms to reestablish cellular homeostasis in response to stressors, TFEB-induced lysosomal biogenesis and enlargement can render cancer cells more vulnerable to compounds targeting lysosomes. This vulnerability opens the door for developing new strategies to combat cancers by simultaneously targeting the lysosome and activating TFEB. This study initially aimed to uncover novel pharmacological agents that function as agonists of TFEB and exhibit substantial cytotoxicity against cancer cells. By conducting cell-based drug screening of the Prestwick library, consisting of 1200 Food and Drug Administration (FDA)-approved compounds, we identified two antidepressants, sertraline and indatraline, as potent inducers of TFEB nuclear translocation. Both compounds promoted cholesterol accumulation within lysosomes, resulting in lysosomal membrane permeabilization, disruption of autophagy, and cell death. Molecular docking analysis unveiled that indatraline and sertraline may inhibit cholesterol traffic by binding to the same cavity where cholesterol typically binds to the lysosomal cholesterol transporters, Niemann-Pick type C1 (NPC1) and NPC2. In cancer cells, sertraline and indatraline elicited immunogenic cell death, converting dying cells into prophylactic vaccines that were able to protect against tumor growth in mice. In a therapeutic setting, a single dose of each compound was sufficient to significantly reduce the outgrowth of established tumors in a T cell-dependent manner. These results identify sertraline and indatraline as immunostimulatory agents that operate through a novel mechanism that connects lysosomal cholesterol accumulation to lysosomal membrane permeabilization, ultimately leading to immunogenic cell death. These results support the repositioning of sertraline and indatraline as immunostimulatory agents for cancer treatment and encourage the broadening of this study to other lysosomal cholesterol transport inhibitors
Ebrahim, Roshan. « Biogenesis of lysosomes in macrophages : intracellular pathway of lysosomal membrane protein to lysosomes ». Doctoral thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/3126.
Texte intégralMilioni, Dimitra. « Perméabilisation photocontrôlée de la membrane biologique : étude en systèmes modèles et en cellules ». Phd thesis, Université Pierre et Marie Curie - Paris VI, 2012. http://tel.archives-ouvertes.fr/tel-00833272.
Texte intégralAtakpa, Peace. « Ca2+ signalling between the endoplasmic reticulum and lysosomes ». Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288002.
Texte intégralCrombie, Andrea Rene. « Lysosomal integral membrane protein II, a member of the CD36 gene family : comparative analysis of structure-function relationships / ». Access full-text from WCMC, 1998. http://proquest.umi.com/pqdweb?did=733079741&sid=9&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Texte intégralJohansson, Ann-Charlotte. « Lysosomal Membrane Permeabilization : A Cellular Suicide Stragegy ». Doctoral thesis, Linköpings universitet, Experimentell patologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-11614.
Texte intégralIn the last decade, a tremendous gain in knowledge concerning the molecular events of apoptosis signaling and execution has been achieved. The aim of this thesis was to clarify the role of lysosomal membrane permeabilization and lysosomal proteases, cathepsins, in signaling for apoptosis. We identified cathepsin D as an important factor in staurosporine-induced human fibroblast cell death. After release to the cytosol, cathepsin D promoted mitochondrial release of cytochrome c by proteolytic activation of Bid. Cathepsin D-mediated cleavage of Bid generated two fragments with the apparent molecular mass of 15 and 19 kDa. By sequence analysis, three cathepsin D-specific cleavage sites, Phe24, Trp48, and Phe183, were identified. Moreover, we investigated the mechanism by which cathepsins escape the lysosomal compartment, and found that Bax is translocated from the cytosol to lysosomes upon staurosporine treatment. In agreement with these data, recombinant Bax triggered release of cathepsins from isolated rat liver lysosomes. Conceivably, the Bcl-2 family of proteins may govern release of pro-apoptotic factors from both lysosomes and mitochondria. The importance of lysosomal cathepsins in apoptosis signaling was studied also in oral squamous cell carcinoma cells following exposure to the redox-cycling drug naphthazarin or agonistic anti-Fas antibodies. In this experimental system, cathepsins were released to the cytosol, however, inhibition of neither cathepsin D, nor cysteine cathepsin activity suppressed cell death. Interestingly, cysteine cathepsins still appeared to be involved in activation of the caspase cascade. Cathepsins are often overexpressed and secreted by cancer cells, and it has been reported that extracellular cathepsins promote tumor growth and metastasis. Here, we propose that cathepsin B secreted from cancer cells may suppress cancer cell death by shedding of the Fas death receptor. Defects in the regulation of apoptosis contribute to a wide variety of diseases, such as cancer, neurodegeneration and autoimmunity. Increased knowledge of the molecular details of apoptosis could lead to novel, more effective, treatments for these illnesses. This thesis emphasizes the importance of the lysosomal death pathway, which is a promising target for future therapeutic intervention.
Ménorval, Marie-Amélie de. « Etude de la perméabilisation de la membrane plasmique et des membranes des organites cellulaires par des agents chimiques et physiques ». Thesis, Paris 11, 2013. http://www.theses.fr/2013PA114840/document.
Texte intégralIt is possible to permeabilize the cellular plasma membrane by using chemical agents (as polyethylen glycols or diméthylsulfoxyde) or physical agents (as ulstrasounds or electric pulses). This permeabilization can be reversible or not, meaning that after the permeabilization, the membrane recovers its integrity and its hemi-permeable properties. These techniques can be used for the uptake of medicines or nucleic acids or to generate cellular fusions. A recent approach, the molecular dynamics, uses numerical simulations to predict the effects of permeabilizing agents at the molecular scale, allowed generating of new data to understand the molecular mechanisms that are not completely known yet.The pulses so called “classical” in electropermeabilization, from the range of the ten of milliseconds to the hundred of microseconds and with a field amplitude in the range of 100 kV/m, can only permeabilize the plasma membrane. However, more recently, shorter pulses, so called nanopulses (few nanosecondes) and with an higher field amplitude (in the range of 10 MV/m) have been used and allow to affect also cellular organelles membranes.This thesis is, in a first time, about the permeabilizing effects of a chemical gent (the diméthylsulfoxyde, DMSO) by comparing predictive models from molecular dynamics with experiments in vitro on cells. The numerical model predicts three regimes of action depending on the DMSO concentration. Used at low concentration, there is a plasma membrane deformation. The use of an intermediate concentration lead to membrane pores formation and higher DMSO concentrations resulted in membrane destruction. The experiments done in vitro on cells confirmed these results using the following of permeabilization markers. This study has been compared to permeabilization due to a physical agent (electric pulses).Secondly, it is about the development and the use of a new cell exposure device for nanopulses that permit to apply very high electric fields and to observe induced cellular effects simultaneously by microscopy.To finish, this device has been used with nanopulses to generate calcium peaks in mesenchymal stem cells that are presenting spontaneous calcium oscillations in correlation to their differentiation state.. These induced peaks are due to the release of the calcium stored in organelles and/or to plasma membrane permeabilization leading to a intramembrane calcium flux establishment. It is also possible to use microsecond pulses to generate calcium peaks in these cells. In this case, the calcium peaks are due to the plasma membrane permeabilization . By changing the amplitude of the applied electric fields and the presence or the absence of external calcium, it is possible to manipulate cytosolic calcium concentrations by mobilizing internal or external calcium. One feature of these new tools is to be triggered and stopped instantly without reminiscence, unlike chemical molecules permitting the production of calcium peaks. These tools could therefore lead to a better understanding of the involvement of calcium in mechanisms such as differentiation, migration or fertilization
Johansson, Ann-Charlotte. « Lysosomal membrane permeabilization : a cellular suicide strategy / ». Linköping : Department of Clinical and Experimental Medicine, Linköping University, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-11614.
Texte intégralTrainito, Claudia. « Study of cell membrane permeabilization induced by pulsed electric field – electrical modeling and characterization on biochip ». Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLN008/document.
Texte intégralThe increasing interest for new methodologies based on the use of the electric field to characterize the cells or tissue cells and generate brought promising development in research laboratories and industry: cancer diagnosis, electrochemotherapy (insertion of a drug after cell membranes permeabilization), gene therapy (insertion of a therapeutic gene), immunotherapy (anti-tumor vaccines obtained by electrofusion of dendritic cells and cancer cells to activate the immune system).The application of electrical pulses to cells or cell tissues induces a change in their properties, in particular on their membranes which become transiently permeable, and temporarily allow the passage of ions and macromolecules. Effect linked to the permeabilization phenomenon have been partially characterized by epi-fluorescence microscopy. Nevertheless, in order to perform the real-time monitoring of the electroporation process and know its dynamics, the electrical sample characterization is employed. Thus the aim of this work is to implement a real-time monitoring of dielectrical characteristics changes, on a wide frequency range, of a cellular tissue or a single cell, before, during and after the pulsed electric field application.As part of my thesis a model of the biological system has been developed to better describe the phenomena observed experimentally: effect of electrical stress on cell viability, on the permeability of the outer membrane, induced effects on the intracellular compounds, dynamics of membrane fusion.The degree of permeabilization of the biological sample (cells or tissues) is non linearly dependent of several parameters, which makes complicated the development of the model and its interpretation.The detection of a specific level of permeabilization is done in real time (measure of the level of permeabilization before, during and after the electric pulses application). This cell permeabilization level control could eventually be parallelized on a chip dedicated to the electroporation of a large number of cells. The latter can be used to optimize the electric pulses parameters in order to reach the desired permeabilization level. In order to have a multi-scale overview of the phenomenon, the study was performed on different size-level: from the tissue level (millimeter scale) to the single cell model through the intermediate scales (cell spéroides characterization).In the latter two cases (spheroid, single cell) the biological sample is isolated in a microfluidic biochip where the electric field solicitation are applied (micrometer scale).The microdevice designed and fabricated during this work, allows the real time characterization of the cell permeabilization. Furthermore the miniaturization of the system is crucial to work at the level of the single cell, and make possible the application of electrical fields of high amplitude, high frequency and spatially localized
Kotnik, Tadej. « Influence de la dynamique du champ électrique sur l'efficacité de l'électroperméabilisation de la membrane cellulaire ». Paris 11, 2000. http://www.theses.fr/2000PA11T026.
Texte intégralLivres sur le sujet "Perméabilisation de la membrane des lysosomes"
Andrade, Luciana. Lysosomes and Membrane Function. Elsevier Science & Technology, 2019.
Trouver le texte intégralDaems, W. Th, E. H. Burger et B. A. Afzelius. Cell Biological Aspects of Disease : The Plasma Membrane and Lysosomes. Springer Netherlands, 2011.
Trouver le texte intégralChapitres de livres sur le sujet "Perméabilisation de la membrane des lysosomes"
Holtzman, Eric. « Acidification ; Membrane Properties ; Permeability and Transport ». Dans Lysosomes, 93–160. Boston, MA : Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_3.
Texte intégralSingh, Rajesh K., et Abigail S. Haka. « Lysosome Exocytosis and Membrane Repair ». Dans Lysosomes : Biology, Diseases, and Therapeutics, 63–85. Hoboken, NJ, USA : John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118978320.ch5.
Texte intégralRepnik, Urška, et Boris Turk. « Lysosomal Membrane Permeabilization in Cell Death ». Dans Lysosomes : Biology, Diseases, and Therapeutics, 115–35. Hoboken, NJ, USA : John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118978320.ch8.
Texte intégralDice, J. Fred. « Selective Degradation of Cytosolic Proteins by Lysosomes ». Dans Molecular Mechanisms of Membrane Traffic, 335–38. Berlin, Heidelberg : Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02928-2_70.
Texte intégralLuzio, J. Paul, Tomomi Kuwana et Barbara M. Mullock. « Signals for Transport from Endosomes to Lysosomes ». Dans Molecular Mechanisms of Membrane Traffic, 351–58. Berlin, Heidelberg : Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02928-2_72.
Texte intégralWood, Salli A., et William J. Brown. « The Morphology but Not the Function of Endosomes and Lysosomes is Affected by Brefeldin A ». Dans Molecular Mechanisms of Membrane Traffic, 367–70. Berlin, Heidelberg : Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02928-2_75.
Texte intégralD’Azzo, A., N. Gillemans et N. Galjart. « The Complex of β-Galactosidase, Neuraminidase and “Protective Protein” in Lysosomes : Molecular Characterization of the “Protective Protein” ». Dans Molecular Basis of Membrane-Associated Diseases, 371–78. Berlin, Heidelberg : Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74415-0_31.
Texte intégralde Chastellier, Chantal, Claude Fréhel et Thierry Lang. « Intracellular Growth of Mycobacterium Avium in Macrophages : Consequences on Membrane Traffic and Exchange of Contents between Endosomes, Lysosomes and Phagosomes ». Dans Endocytosis, 375–80. Berlin, Heidelberg : Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_47.
Texte intégralIsenman, Lois. « Selective secretion by lysosomes ». Dans Membrane Protein Transport, 145–67. Elsevier, 1995. http://dx.doi.org/10.1016/s1874-592x(06)80021-1.
Texte intégralCorrotte, Matthias, et Thiago Castro-Gomes. « Lysosomes and plasma membrane repair ». Dans Current Topics in Membranes, 1–16. Elsevier, 2019. http://dx.doi.org/10.1016/bs.ctm.2019.08.001.
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