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Статті в журналах з теми "Perméabilisation de la membrane des lysosomes"
1
Haylett, T., and L. Thilo. "Limited and selective transfer of plasma membrane glycoproteins to membrane of secondary lysosomes." Journal of Cell Biology 103, no. 4 (October 1, 1986): 1249–56. http://dx.doi.org/10.1083/jcb.103.4.1249.
Повний текст джерелаАнотація:
Radioactive galactose, covalently bound to cell surface glycoconjugates on mouse macrophage cells, P388D1, was used as a membrane marker to study the composition, and the kinetics of exchange, of plasma membrane-derived constituents in the membrane of secondary lysosomes. Secondary lysosomes were separated from endosomes and plasma membrane on self-forming Percoll density gradients. Horseradish peroxidase, taken up by fluid-phase pinocytosis, served as a vesicle contents marker to monitor transfer of endosomal contents into secondary lysosomes. Concurrently, the fraction of plasma membrane-derived label in secondary lysosomes increased by first order kinetics (k = [56 min]-1) from less than 0.1% (background level) to a steady-state level of approximately 2.5% of the total label. As analyzed by NaDodSO4 PAGE, labeled molecules of Mr 160-190 kD were depleted and of Mr 100-120 kD were enriched in lysosome membrane compared with the relative composition of label on the cell surface. No corresponding selectivity was observed for the degradation of label, with all Mr classes being affected to the same relative extent. The results indicate that endocytosis-derived transfer of plasma membrane constituents to secondary lysosomes is a limited and selective process, and that only approximately 1% of internalized membrane is recycled via a membrane pool of secondary lysosomes.
2
Luzio, J. Paul, Paul R. Pryor, Sally R. Gray, Matthew J. Gratian, Robert C. Piper, and Nicholas A. Bright. "Membrane traffic to and from lysosomes." Biochemical Society Symposia 72 (January 1, 2005): 77–86. http://dx.doi.org/10.1042/bss0720077.
Повний текст джерелаАнотація:
In the late endocytic pathway, it has been proposed that endocytosed macromolecules are delivered to a proteolytic environment by 'kiss-and-run' events or direct fusion between late endosomes and lysosomes. To test whether the fusion hypothesis accounts for delivery to lysosomes in living cells, we have used confocal microscopy to examine content mixing between lysosomes loaded with rhodamine-dextran and endosomes subsequently loaded with Oregon-Green-dextran. Both kissing and explosive fusion events were recorded. Data from cell-free content-mixing assays have suggested that fusion is initiated by tethering, which leads to formation of a trans-SNARE (soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor) protein complex and then release of lumenal Ca2+, followed by membrane bilayer fusion. We have shown that the R-SNARE (arginine-containing SNARE) protein VAMP (vesicle-associated membrane protein) 7 is necessary for heterotypic fusion between late endosomes and lysosomes, whereas a different R-SNARE, VAMP 8 is required for homotypic fusion of late endosomes. After fusion of lysosomes with late endosomes, lysosomes are re-formed from the resultant hybrid organelles, a process requiring condensation of content and the removal/recycling of some membrane proteins.
3
Andrews, Norma W. "Lysosomes and the plasma membrane." Journal of Cell Biology 158, no. 3 (July 29, 2002): 389–94. http://dx.doi.org/10.1083/jcb.200205110.
Повний текст джерелаАнотація:
Studies of the cell invasion mechanism of the parasite Trypanosoma cruzi led to a series of novel findings, which revealed a previously unsuspected ability of conventional lysosomes to fuse with the plasma membrane. This regulated exocytic process, previously regarded mostly as a specialization of certain cell types, was recently shown to play an important role in the mechanism by which cells reseal their plasma membrane after injury.
4
Green, S. A., K. P. Zimmer, G. Griffiths, and I. Mellman. "Kinetics of intracellular transport and sorting of lysosomal membrane and plasma membrane proteins." Journal of Cell Biology 105, no. 3 (September 1, 1987): 1227–40. http://dx.doi.org/10.1083/jcb.105.3.1227.
Повний текст джерелаАнотація:
We have used monospecific antisera to two lysosomal membrane glycoproteins, lgp120 and a similar protein, lgp110, to compare the biosynthesis and intracellular transport of lysosomal membrane components, plasma membrane proteins, and lysosomal enzymes. In J774 cells and NRK cells, newly synthesized lysosomal membrane and plasma membrane proteins (the IgG1/IgG2b Fc receptor or influenza virus hemagglutinin) were transported through the Golgi apparatus (defined by acquisition of resistance to endo-beta-N-acetylglucosaminidase H) with the same kinetics (t1/2 = 11-14 min). In addition, immunoelectron microscopy of normal rat kidney cells showed that lgp120 and vesicular stomatitis virus G-protein were present in the same Golgi cisternae demonstrating that lysosomal and plasma membrane proteins were not sorted either before or during transport through the Golgi apparatus. To define the site at which sorting occurred, we compared the kinetics of transport of lysosomal and plasma membrane proteins and a lysosomal enzyme to their respective destinations. Newly synthesized proteins were detected in dense lysosomes (lgp's and beta-glucuronidase) or on the cell surface (Fc receptor or hemagglutinin) after the same lag period (20-25 min), and accumulated at their final destinations with similar kinetics (t1/2 = 30-45 min), suggesting that these two lgp's are not transported to the plasma membrane before reaching lysosomes. This was further supported by measurements of the transport of membrane-bound endocytic markers from the cell surface to lysosomes, which exhibited additional lag periods of 5-15 min and half-times of 1.5-2 h. The time required for transport of newly synthesized plasma membrane proteins to the cell surface, and for the transport of plasma membrane markers from the cell surface to lysosomes would appear too long to account for the rapid transport of lgp's from the Golgi apparatus to lysosomes. Thus, the observed kinetics suggest that lysosomal membrane proteins are sorted from plasma membrane proteins at a post-Golgi intracellular site, possibly the trans Golgi network, before their delivery to lysosomes.
5
Toyomura, Takao, Yoshiko Murata, Akitsugu Yamamoto, Toshihiko Oka, Ge-Hong Sun-Wada, Yoh Wada, and Masamitsu Futai. "From Lysosomes to the Plasma Membrane." Journal of Biological Chemistry 278, no. 24 (April 2, 2003): 22023–30. http://dx.doi.org/10.1074/jbc.m302436200.
Повний текст джерела
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Blott, Emma J., Giovanna Bossi, Richard Clark, Marketa Zvelebil, and 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 (July 1, 2001): 2405–16. http://dx.doi.org/10.1242/jcs.114.13.2405.
Повний текст джерелаАнотація:
Fas ligand (FasL) induces apoptosis through its cell surface receptor Fas. T lymphocytes and natural killer cells sort newly synthesised FasL to secretory lysosomes but, in cell types with conventional lysosomes, FasL appears directly on the plasma membrane. Here, we define a proline-rich domain (PRD) in the cytoplasmic tail of FasL that is responsible for sorting FasL to secretory lysosomes. Deletion of this PRD results in cell surface expression of FasL in cells with secretory lysosomes. Positively charged residues flanking the PRD are crucial to the sorting motif and changing the charge of these residues causes mis-sorting to the plasma membrane. In cells with conventional lysosomes, this motif is not recognised and FasL is expressed at the plasma membrane. The FasL PRD is not required for endocytosis in any cell type, as deletion mutants lacking this motif are endocytosed efficiently to the lysosomal compartment. Endogenous FasL cannot internalise extracellular antibody, demonstrating that FasL does not transit the plasma membrane en route to the secretory lysosomes. We propose that an interaction of the PRD of FasL with an SH3-domain-containing protein, enables direct sorting of FasL from the Golgi to secretory lysosomes.
7
Jaiswal, Jyoti K., Norma W. Andrews, and 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 (November 18, 2002): 625–35. http://dx.doi.org/10.1083/jcb.200208154.
Повний текст джерелаАнотація:
Similar to its role in secretory cells, calcium triggers exocytosis in nonsecretory cells. This calcium-dependent exocytosis is essential for repair of membrane ruptures. Using total internal reflection fluorescence microscopy, we observed that many organelles implicated in this process, including ER, post-Golgi vesicles, late endosomes, early endosomes, and lysosomes, were within 100 nm of the plasma membrane (in the evanescent field). However, an increase in cytosolic calcium led to exocytosis of only the lysosomes. The lysosomes that fused were predominantly predocked at the plasma membrane, indicating that calcium is primarily responsible for fusion and not recruitment of lysosomes to the cell surface.
8
WAN, Feng-Yi, Yi-Nan WANG, and Guo-Jiang ZHANG. "The influence of oxidation of membrane thiol groups on lysosomal proton permeability." Biochemical Journal 360, no. 2 (November 26, 2001): 355–62. http://dx.doi.org/10.1042/bj3600355.
Повний текст джерелаАнотація:
The influence of oxidation of membrane thiol groups on lysosomal proton permeability was studied by measuring lysosomal pH with FITC-conjugated dextran, determining the membrane potential with 3,3′-dipropylthiadicarbocyanine iodide and monitoring their proton leakage with p-nitrophenol. Residual membrane thiol groups were measured with 5,5′-dithiobis-(2-nitrobenzoic acid). The lysosomal membrane thiol groups were modified by treatment with diamide and dithiothreitol. SDS/PAGE revealed aggregations of the membrane proteins induced by the treatment of lysosomes with diamide. The cross-linkage of proteins could be abolished by subsequent treatment with dithiothreitol, indicating that the proteins were linked via disulphide bonds. Treating the lysosomes with diamide decreased their membrane thiol groups and caused increases in lysosomal pH, membrane potential and proton leakage, which could be reversed by treatment of the lysosomes with dithiothreitol. This indicates that the lysosomal proton permeability can be increased by oxidation of the membrane thiol groups and restored to the normal level by reduction of the groups. Treatment of the lysosomes with N-ethylmaleimide reduced their membrane thiol groups but did not change the lysosomal pH or their degree of proton leakage. It suggests that protein aggregation may be an important mechanism for the increase in lysosomal proton permeability. The results raise the possibility that the proton permeability of lysosomes in vivo may be affected by the redox states of their membrane thiol groups.
9
Rodríguez, Ana, Paul Webster, Javier Ortego, and Norma W. Andrews. "Lysosomes Behave as Ca2+-regulated Exocytic Vesicles in Fibroblasts and Epithelial Cells." Journal of Cell Biology 137, no. 1 (April 7, 1997): 93–104. http://dx.doi.org/10.1083/jcb.137.1.93.
Повний текст джерелаАнотація:
Lysosomes are considered to be a terminal degradative compartment of the endocytic pathway, into which transport is mostly unidirectional. However, specialized secretory vesicles regulated by Ca2+, such as neutrophil azurophil granules, mast cell–specific granules, and cytotoxic lymphocyte lytic granules, share characteristics with lysosomes that may reflect a common biogenesis. In addition, the involvement of Ca2+ transients in the invasion mechanism of the parasite Trypanosoma cruzi, which occurs by fusion of lysosomes with the plasma membrane, suggested that lysosome exocytosis might be a generalized process present in most cell types. Here we demonstrate that elevation in the intracellular free Ca2+ concentration of normal rat kidney (NRK) fibroblasts induces fusion of lysosomes with the plasma membrane. This was verified by measuring the release of the lysosomal enzyme β-hexosaminidase, the appearance on the plasma membrane of the lysosomal glycoprotein lgp120, the release of fluid-phase tracers previously loaded into lysosomes, and the release of the lysosomally processed form of cathepsin D. Exposure to the Ca2+ ionophore ionomycin or addition of Ca2+containing buffers to streptolysin O–permeabilized cells induced exocytosis of ∼10% of the total lysosomes of NRK cells. The process was also detected in other cell types such as epithelial cells and myoblasts. Lysosomal exocytosis was found to require micromolar levels of Ca2+ and to be temperature and ATP dependent, similar to Ca2+-regulated secretory mechanisms in specialized cells. These findings highlight a novel role for lysosomes in cellular membrane traffic and suggest that fusion of lysosomes with the plasma membrane may be an ubiquitous form of Ca2+-regulated exocytosis.
10
Draye, J. P., P. J. Courtoy, J. Quintart, and 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 (December 1, 1988): 2109–15. http://dx.doi.org/10.1083/jcb.107.6.2109.
Повний текст джерелаАнотація:
We present here a mathematical model that accounts for the various proportions of plasma membrane constituents occurring in the lysosomal membrane of rat fibroblasts (Draye, J.-P., J. Quintart, P. J. Courtoy, and P. Baudhuin. 1987. Eur. J. Biochem. 170: 395-403; Draye, J.-P., P. J. Courtoy, J. Quintart, and P. Baudhuin. 1987. Eur. J. Biochem. 170:405-411). It is based on contents of plasma membrane markers in purified lysosomal preparations, evaluations of their half-life in lysosomes and measurements of areas of lysosomal and plasma membranes by morphometry. In rat fibroblasts, structures labeled by a 2-h uptake of horseradish peroxidase followed by a 16-h chase (i.e., lysosomes) occupy 3% of the cellular volume and their total membrane area corresponds to 30% of the pericellular membrane area. Based on the latter values, the model predicts the rate of inflow and outflow of plasma membrane constituents into lysosomal membrane, provided their rate of degradation is known. Of the bulk of polypeptides iodinated at the cell surface, only 4% reach the lysosomes every hour, where the major part (integral of 83%) is degraded with a half-life in lysosomes of integral to 0.8 h. For specific plasma membrane constituents, this model can further account for differences in the association to the lysosomal membrane by variations in the rate either of lysosomal degradation, of inflow along the pathway from the pericellular membrane to the lysosomes, or of lateral diffusion.
Дисертації з теми "Perméabilisation de la membrane des lysosomes"
1
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.
Повний текст джерелаАнотація:
Les lysosomes jouent un rôle central dans la régulation des processus anaboliques et cataboliques, la signalisation cellulaire ainsi que dans la mise en œuvre des programmes transcriptionnels au sein des cellules. Ils favorisent l’adaptation des cellules cancéreuses lors des variations du microenvironnement en leur fournissant les métabolites essentiels et l’énergie nécessaire à leur survie et à leur prolifération. Un acteur majeur dans la réponse adaptative des lysosomes est le facteur de transcription EB (TFEB). TFEB coordonne l’expression de gènes associés à la fonction et à la biogenèse des lysosomes, y compris ceux impliqués dans l’autophagie, un processus catabolique majeur des cellules qui dépend des lysosomes. TFEB et l’autophagie fonctionnent comme des mécanismes adaptatifs visant à rétablir l’homéostasie cellulaire en réponse à un stress. Cependant, la biogenèse des lysosomes et l'augmentation de leur taille induite par TFEB peuvent rendre les cellules cancéreuses plus vulnérables aux composés ciblant les lysosomes. Cette vulnérabilité ouvre la porte au développement de nouvelles stratégies pour lutter contre le cancer en ciblant simultanément les lysosomes et en activant TFEB. L’objectif initial de cette étude a été de découvrir de nouveaux agents pharmacologiques agonistes de TFEB, manifestant une cytotoxicité significative contre les cellules cancéreuses. Par un criblage de la bibliothèque Prestwick comprenant 1200 composés approuvés par la « Food and Drug Administration » (FDA), nous avons identifié deux antidépresseurs, la sertraline et l’indatraline, qui agissent en tant que puissants activateurs de la translocation de TFEB vers le noyau. Les deux composés induisent une accumulation de cholestérol au sein des lysosomes, entraînant la perméabilisation de leurs membranes et une perturbation du flux autophagique. L’analyse de modélisation moléculaire a révélé que les deux composés pourraient inhiber le trafic du cholestérol en se liant au site de fixation du cholestérol des transporteurs, Niemann-Pick type C1 (NPC1) et NPC2. Dans les cellules cancéreuses, la sertraline et l’indatraline provoquent une mort cellulaire immunogénique, en transformant les cellules mourantes en vaccins prophylactiques capables de protéger contre la croissance tumorale chez la souris. Dans un contexte thérapeutique, une dose unique de ces composés était suffisante pour ralentir de façon significative la croissance tumorale de manière dépendante des lymphocytes T. Ces résultats caractérisent la sertraline et l’indatraline comme des agents immunostimulants qui agissent à travers un mécanisme novateur connectant l’accumulation du cholestérol lysosomal aux dommages lysosomaux, entraînant ainsi la mort immunogénique des cellules cancéreuses. Ces résultats soutiennent le repositionnement de ces deux molécules en tant qu’agents immunostimulants pour le traitement du cancer et encouragent l’extension de cette étude à d’autres inhibiteurs du transport lysosomal du cholestérolLysosomes 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
2
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.
Повний текст джерела
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Milioni, 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.
Повний текст джерелаАнотація:
La perméabilisation de la membrane lipidique est actuellement un domaine de recherche important, puisque l'optimisation du transport des petites molécules (comme l'ADN ou les protéines) dans les cellules est nécessaire. Dans ce travail, nous tentons une contribution dans ce domaine en proposant une méthode de perméabilisation contrôlée à l'aide des Azobenzene Modified Polymers (AMP). Des copolymères avec un taux d'hydrophobicité modéré ont été montrés dans le passé comme perméabilisant la membrane. Les AMP nous permettraient alors de contrôler cette perméabilisation via le contrôle de leur taux d'hydrophobicité (selon la longueur d'onde de la lumière à laquelle ils sont illuminés). Cette hypothèse a été vérifiée à l'aide des vésicules géantes unilamellaires (GUV) encapsulant des sondes fluorescentes solubles. La cinétique de la fuite de ces sondes en combinaison avec des expériences d'électrophysiologie sur des films noirs (BLM) nous donne accès à une meilleure caractérisation des structures de perméation créées par l'interaction entre l'AMP et les lipides. En outre, des expériences ont été réalisées sur des cellules CHO (Chinese Hamster Overy). La possibilité de faire rentrer dans les cellules des molécules qui a priori n'y sont pas internalisées a été étudiée. Par ailleurs, la fuite de molécules encapsulées dans les cellules et sa cinétique ont été examinées
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Atakpa, Peace. "Ca2+ signalling between the endoplasmic reticulum and lysosomes." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288002.
Повний текст джерелаАнотація:
Ca2+ is a universal and versatile intracellular messenger, regulating a vast array of biological processes due to variations in the frequency, amplitude, spatial and temporal dynamics of Ca2+ signals. Increases in cytosolic free Ca2+ concentration ([Ca2+]c) are due to influx from either an infinite extracellular Ca2+ pool or from the more limited intracellular Ca2+ stores. Stimulation of the endogenous muscarinic (M3) receptors of human embryonic kidney (HEK) cells with carbachol results in the activation of phospholipase C (PLC) and formation of inositol 1,4,5-trisphosphate (IP3), activation of IP3 receptors (IP3Rs), release of Ca2+ from the endoplasmic reticulum (ER), and activation of store-operated Ca2+ entry (SOCE). Lysosomes are the core digestive compartments of the cell, but their importance as signalling organelles is also now widely appreciated. Accumulating evidence indicates that lysosomal Ca2+ is important for their physiological functions. Lysosomal Ca2+ release triggers fusion during membrane trafficking and, through calmodulin, it regulates lysosome size. Luminal Ca2+ is critical for regulation of lysosomal biogenesis and autophagy during starvation through the transcription factor, TFEB. Furthermore, aberrant lysosomal Ca2+ is associated with some lysosomal storage diseases. Lysosomes in mammalian cells have long been suggested to accumulate Ca2+ via a low-affinity Ca2+-H+ exchanger (CAX). This is consistent with evidence that dissipating the lysosomal H+ gradient increased [Ca2+]c and decreased lysosomal free [Ca2+], and with the observation that lysosomal Ca2+ uptake was followed by an increase in pHly. Furthermore, heterologous expression of Xenopus CAX in mammalian cells attenuated carbachol-evoked Ca2+ signals. However, there is no known CAX in mammalian cells, and so the identity of the lysosomal Ca2+ uptake pathway in mammalian cells is unresolved. Using mammalian cells loaded with a fluorescent Ca2+ indicator, I show that dissipating the pHly gradient pharmacologically or by siRNA-mediated knockdown of an essential subunit of the H+ pump, increases the amplitude of IP3-evoked cytosolic Ca2+ signals without affecting those evoked by SOCE. A genetically encoded low-affinity Ca2+ sensor expressed on the lysosome surface reports larger increases in [Ca2+]c than the cytosolic sensor, but only when the Ca2+ signals are evoked by IP3R rather than SOCE. Using cells expressing single IP3R subtypes, I demonstrate that each of the three IP3R subtypes can deliver Ca2+ to lysosomes. I conclude that IP3Rs release Ca2+ within near-lysosome microdomains that fuel a low-affinity lysosomal Ca2+ uptake system. The temporal relationship between the increase in pHly and reduced Ca2+ sequestration suggests that pHly affects the organization of the microdomain rather than the Ca2+ uptake mechanism. I show that abrogation of the lysosome H+ gradient does not acutely prevent uptake of Ca2+ into lysosomes, but disrupts junctions with the ER where the exchange of Ca2+ occurs. The dipeptide, glycyl-L-phenylalanine 2-naphthylamide (L-GPN), is much used to disrupt lysosomes and release Ca2+ from them. The mechanism is widely assumed to require cleavage of GPN by cathepsin C, causing accumulation of amino acid residues, and osmotic lysis of lysosomal membranes. I show, using LysoTracker Red and Oregon Green-dextran to report pHly, that L-GPN is effective in HEK cells lacking functional cathepsin C, following CRISPR-Cas9-mediated gene disruption. Furthermore, D-GPN, which is resistant to cleavage by cathepsin C, is as effective as L-GPN at increasing pHly, and it is similarly effective in cells with and without cathepsin C. L-GPN and D-GPN increase cytosolic pH, and the effect is similar when the lysosomal V-ATPase is inhibited with bafilomycin A1. This is not consistent with GPN releasing the acidic contents of lysosomes. I conclude that the effects of GPN on lysosomes are not mediated by cathepsin C. Both L-GPN and D-GPN evoke Ca2+ release, the response is unaffected by inhibition or knock-out of cathepsin C, but it requires Ca2+ within the ER. GPN-evoked increases in [Ca2+]c require Ca2+ within the ER, but they are not mediated by ER Ca2+ channels amplifying Ca2+ release from lysosomes. GPN increases [Ca2+]c by increasing pHcyt, which then directly stimulates Ca2+ release from the ER. I conclude that physiologically relevant increases in pHcyt stimulate Ca2+ release from the ER independent of IP3 and ryanodine receptors, and that GPN does not selectively target lysosomes. I conclude that all three IP3R subtypes selectively deliver Ca2+ to lysosomes, and that the low pH within lysosomes is required to maintain the junctions between ER and lysosomes, but not for lysosomal Ca2+ uptake. I suggest that GPN lacks the specificity required to allow selective release of Ca2+ from lysosomes.
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Crombie, 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.
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Johansson, 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.
Повний текст джерелаАнотація:
In 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.In 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.
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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.
Повний текст джерелаАнотація:
Il est possible de perméabiliser la membrane plasmique des cellules par des agents chimiques (tels que les polyéthylènes glycols ou le diméthylsulfoxyde) ou par des agents physiques (tels que les ultrasons ou les impulsions électriques). Cette perméabilisation peut être réversible ou non, ce qui signifie qu’après la perméabilisation, la membrane retrouve son intégrité et ses propriétés d’hémi-perméabilité ou pas. Ces techniques peuvent être utilisées pour faire rentrer des médicaments ou des acides nucléiques dans les cellules ou pour générer des fusions cellulaires. Une approche récente, la dynamique moléculaire, utilise des simulations numériques pour prédire les effets des agents perméabilisants sur les membranes à l’échelle moléculaire, et permet d’apporter de nouvelles données pour comprendre les mécanismes moléculaires, encore peu connus à ce jour.Les impulsions dites « classiques » en électroperméabilisation, de l’ordre de la dizaine de millisecondes à la centaine de microsecondes et d’amplitude de champ de l’ordre de 100 kV/m, perméabilisent la membrane plasmique uniquement. Cependant, récemment, des impulsions plus courtes, dites impulsions nanoseconde (quelques nanosecondes) et de plus grande amplitude de champ (de l’ordre de 10 MV/m) ont été utilisées et permettent d’affecter également les membranes des organites cellulaires. Les travaux de cette thèse portent dans un premier temps sur les effets perméabilisants d’un agent chimique (le diméthylsulfoxyde, DMSO) en comparant les modèles prédictifs de la dynamique moléculaire avec des expériences in vitro sur des cellules. Le modèle numérique prédit trois régimes d’action en fonction de la concentration du DMSO. Utilisé à faible concentration, il y a déformation de la membrane plasmique. L’utilisation d’une concentration intermédiaire entraîne la formation de pores membranaires et les fortes concentrations de DMSO ont pour conséquence la destruction de la membrane. Les expériences in vitro faites sur des cellules ont confirmé ces résultats en suivant l’entrée de marqueurs de perméabilisation. Cette étude a été comparée avec la perméabilisation par un agent physique (les impulsions électriques). Dans un deuxième temps, ces travaux traitent du développement et de l’utilisation d’un nouveau dispositif d’exposition des cellules aux impulsions nanoseconde qui permet d’appliquer des champs électriques très élevés et d’observer par microscopie leurs au niveau cellulaire. Pour finir, ce dispositif a été utilisé avec des impulsions nanoseconde pour générer des pics calciques dans de cellules souches mésenchymateuses qui présentent des oscillations calciques spontanées liées à leur état de différenciation. Ces pics induits sont dus à la libération de calcium stocké dans les organites et/ou à la perméabilisation de la membrane plasmique permettant l’établissement d’un flux de calcium intramembranaire. Il est aussi possible d’utiliser des impulsions microseconde pour générer des pics calciques dans ces cellules. Dans ce cas, les pics calciques ne sont dus qu’à la perméabilisation de la membrane plasmique. En jouant sur l’amplitude des champs électriques appliqués et sur la présence ou l’absence de calcium externe, il est possible de manipuler les concentrations calciques cytosoliques en mobilisant le calcium interne ou externe. Une des particularités de ces nouveaux outils est de pouvoir être déclenchés et arrêtés instantanément, sans réminiscence, contrairement aux molécules chimiques permettant de produire des pics calciques. Ces outils pourraient donc permettre de mieux comprendre l’implication du calcium dans des mécanismes comme la différenciation, la migration ou la fécondationIt 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
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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.
Повний текст джерела
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Trainito, 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.
Повний текст джерелаАнотація:
Depuis plusieurs années, de nouvelles méthodologies basées sur l’utilisation du champ électrique pour agir ou caractériser les cellules ou les tissus cellulaires génèrent de nombreuses avancées et apportent des nouvelles promesses dans les laboratoires de recherche et dans l'industrie : diagnostic de cancer, ElectroChimioThérapie (insertion d’un médicament en perméabilisant les membranes des cellules), thérapie génique (insertion d’un gène thérapeutique), immunothérapie (vaccins anti-tumoraux obtenus par électrofusion de cellules dendritiques et cellules cancéreuses pour réactiver le système immunitaire).L’application d’ impulsions électriques à des cellules ou dans des tissus cellulaires induit un changement sur leurs propriétés, en particulier sur leurs membranes qui deviennent transitoirement perméables, laissant temporairement le passage aux ions et macro-molécules. Les phénomènes induits lors d’une perméabilisation par application de champ électrique ont été partiellement caractérisés en microscopie epi-fluorescence. Pour effectuer un suivi en temps réel de la dynamique du processus de l’électroperméabilisation, une voie prometteuse consiste à caractériser électriquement l’échantillon. Dans cet objectif, mon travail de thèse consiste à mettre en oeuvre le suivi en temps réel de l’évolution des caractéristiques électriques sur une large bande de fréquences d’un tissu cellulaire ou d’une cellule isolée, avant, pendant et après la sollicitation par un champ électrique pulsé.Dans le cadre de ma thèse un modèle du système biologique et de son environnement a été élaboré, afin de mieux décrire des phénomènes observés expérimentalement: effet des sollicitations électriques sur la viabilité cellulaire, sur la perméabilité de la membrane externe, effets induits sur les composés intracellulaires, dynamique de fusion membranaire. Le degré de perméabilisation de l’objet biologique (cellule ou tissu) dépend de manière fortement non-linéaire de nombreux paramètres, ce qui rend complexe l’élaboration de ce modèle et son interprétation. La détection de ce niveau de perméabilisation est effectuée en temps réel (mesure du niveau de perméabilisation avant, pendant et après l’application de l’impulsion électrique). In fine cette approche devrait permettre d’optimiser le taux de perméabilisation cellulaire en fonction de l’application considérée. Ce système de contrôle individuel du niveau de perméabilisation cellulaire pourrait à terme être parallélisé massivement sur une puce dédiée à l’électroporation d’un grand nombre de cellules. Afin d’avoir une vision multi-échelle des effets, l’étude a été menée sur plusieurs modèles expérimentaux: qui vont du tissu (échelle millimétrique) à la cellule unique, en passant par les échelles intermédiaires (caractérisation de spéroides cellulaires).Dans ces deux derniers cas (sphéroide, cellule unique) l’objet biologique est isolé dans une biopuce microfluidique équipée d’électrodes de mesure et d’application du champ (échelle micrométrique).Les micro-dispositifs que j’ai réalisé pour caractériser en temps réel la perméabilisation de cellules, intègrent une géométrie spécifique d’électrodes, ainsi que d'un réseau de canaux microfluidiques pour contrôler le débit de cellules Le degré de miniaturisation de ces puces permet de travailler au niveau de la cellule unique, et appliquer des champs électriques de forte amplitude, de forte fréquence, localisés spatialementThe 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
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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.
Повний текст джерелаАнотація:
L'électroperméabilisation est une méthode établie pour permettre l'internalisation des molécules exogènes dans les cellules en suspension et dans les tissus. Dans beaucoup d'applications, expérimentales et cliniques, il est très important que le pourcentage des cellules perméabilisées, le pourcentage des cellules survivantes, et souvent aussi la quantité de molécules internalisées, soient tous aussi élevés que possible. Pour améliorer l'efficacité des protocoles d'électroperméabilisation, le rôle de l'amplitude, de la durée et du nombre d'impulsions ont été étudiés en détail. Par contre, les études de l'influence de la forme de l'impulsion sur l'efficacité de l'électroperméabilisation ont été très rares, ce qui est en partie dû au manque de générateurs d'impulsions de haut voltage d'une forme autre qu'exponentielle ou rectangulaire. Le but principal de la recherche décrite dans cette thèse était d'étudier le rôle de la forme des impulsions dans l'efficacité de l'électroperméabilisation des cellules en suspension. Pour établir une base théorique pour les études expérimentales, nous avons développé une méthode d'analyse du voltage transmembranaire induit par des champs électriques qui varient au cours du temps. Nous avons également analysé le rôle des conductivités du milieu extracellulaire, de la membrane et du cytoplasme, et aussi du rayon et de la forme des cellules sur le voltage transmembranaire induit. Pour générer des impulsions ayant différentes formes, nous avons construit un système composé d'un générateur de fonctions programmable commercial et d'un amplificateur bipolaire à haute fréquence et à haut voltage. Concernant la détermination du pourcentage de cellules électroperméabilisées, nous avons développé une nouvelle méthode basée sur la bléomycine, un agent cytotoxique qui ne peut pas diffuser à travers une membrane plasmique intacte et qui mène ainsi à la mort sélective des cellules perméabilisées. Cette méthode élimine plusieurs des inconvénients de la méthode la plus communément utilisée, celle basée sur l'iodure de propidium. Nos expériences nous permettent de confirmer que pour des impulsions rectangulaires monophasiques, la perméabilisation augmente et la survie diminue avec l'augmentation de la durée et du nombre d'impulsions. Pour l'internalisation des petites molécules exogènes, nous montrons que le nombre d'impulsions joue un rôle plus important que la durée d'impulsion. Nous montrons aussi que la perméabilisation et l'internalisation des petites molécules exogènes provoquées par les impulsions biphasiques sont augmentées par rapport à des impulsions monophasiques de durée et d'amplitude identiques. Par contre, la survie obtenue avec des impulsions biphasiques est très similaire à celle réalisée par des impulsions monophasiques. Ces effets peuvent être expliqués sur la base de l'asymétrie du voltage transmembranaire total en raison du voltage transmembranaire de repos. Les impulsions biphasiques compensent cette asymétrie, et en plus elles permettent de délivrer une charge équilibrée au niveau des électrodes, réduisant la contamination électrolytique. Dans la gamme des temps de montée et de descente des impulsions rectangulaires de 2 µs à 100 µs, nous n'avons trouvé aucune influence de ces temps dans l'efficacité de l'électroperméabilisation. Nos résultats suggèrent aussi qu'un des paramètres très importants pour l'électroperméabilisation est la durée sans interruption pendant laquelle l'impulsion dépasse une certaine intensité critique.
Книги з теми "Perméabilisation de la membrane des lysosomes"
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Andrade, Luciana. Lysosomes and Membrane Function. Elsevier Science & Technology, 2019.
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Daems, W. Th, E. H. Burger, and B. A. Afzelius. Cell Biological Aspects of Disease: The Plasma Membrane and Lysosomes. Springer Netherlands, 2011.
Знайти повний текст джерелаЧастини книг з теми "Perméabilisation de la membrane des lysosomes"
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Holtzman, Eric. "Acidification; Membrane Properties; Permeability and Transport." In Lysosomes, 93–160. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_3.
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Singh, Rajesh K., and Abigail S. Haka. "Lysosome Exocytosis and Membrane Repair." In Lysosomes: Biology, Diseases, and Therapeutics, 63–85. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118978320.ch5.
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Repnik, Urška, and Boris Turk. "Lysosomal Membrane Permeabilization in Cell Death." In Lysosomes: Biology, Diseases, and Therapeutics, 115–35. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118978320.ch8.
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Dice, J. Fred. "Selective Degradation of Cytosolic Proteins by Lysosomes." In 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.
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Luzio, J. Paul, Tomomi Kuwana, and Barbara M. Mullock. "Signals for Transport from Endosomes to Lysosomes." In 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.
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Wood, Salli A., and William J. Brown. "The Morphology but Not the Function of Endosomes and Lysosomes is Affected by Brefeldin A." In 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.
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D’Azzo, A., N. Gillemans, and N. Galjart. "The Complex of β-Galactosidase, Neuraminidase and “Protective Protein” in Lysosomes: Molecular Characterization of the “Protective Protein”." In 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.
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de Chastellier, Chantal, Claude Fréhel, and Thierry Lang. "Intracellular Growth of Mycobacterium Avium in Macrophages: Consequences on Membrane Traffic and Exchange of Contents between Endosomes, Lysosomes and Phagosomes." In Endocytosis, 375–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_47.
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Isenman, Lois. "Selective secretion by lysosomes." In Membrane Protein Transport, 145–67. Elsevier, 1995. http://dx.doi.org/10.1016/s1874-592x(06)80021-1.
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Corrotte, Matthias, and Thiago Castro-Gomes. "Lysosomes and plasma membrane repair." In Current Topics in Membranes, 1–16. Elsevier, 2019. http://dx.doi.org/10.1016/bs.ctm.2019.08.001.
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